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Research progress of serum eosinophil in chronic obstructive pulmonary disease and asthma

  • Congli Wu EMAIL logo
Published/Copyright: December 7, 2023
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Open Life Sciences
From the journal Open Life Sciences Volume 18 Issue 1

Abstract

Chronic obstructive pulmonary disease (COPD) and asthma are common airway diseases, and there are similarities and differences between them. Serum eosinophil (EOS) has potential application value in the diagnosis, treatment, and prognosis of COPD and asthma. However, the clinical application value of serum EOS in these two diseases is controversial. In this work, recent research progress on the application of serum EOS in COPD and asthma was analyzed, and the potential application of serum EOS in the two diseases was expounded from several aspects, including the correlation between the pathogenesis of COPD and asthma and EOS, as well as the correlation between the diagnosis, treatment, and prognosis of the two diseases and serum EOS. The results revealed that serum EOS was important in the pathogenesis, diagnosis, treatment, and prognosis of COPD and asthma and exhibited a potential clinical application value. However, further study was needed to evaluate the threshold, which provided guidance for the clinical diagnosis and treatment of COPD and asthma.

Keywords: eosinophil; chronic obstructive pulmonary disease; asthma; pathogenesis; diagnosis; prognosis

Asthma and chronic obstructive pulmonary disease (COPD) are two common airway diseases. COPD is a chronic respiratory disease characterized by persistent respiratory symptoms and airflow limitation, often caused by airway and/or alveolar abnormalities caused by toxic particles or gases [1]. Asthma is a chronic airway inflammatory disease, which involves a variety of cells and cell components. Asthma and COPD are effectively distinguished due to differences in bronchodilation tests [2]. However, patients with both diseases have clinical symptoms such as cough, phlegm, wheezing, and shortness of breath [3]. Some patients may be characterized by asthma–COPD overlapping (ACO), and about 20% of COPD patients are misdiagnosed as ACO [4]. Some researchers have pointed out that chronic airway diseases are the result of the combined action of genes and environmental factors and believe that asthma and COPD are two different manifestations of the same disease [5]. Approximately one-third of patients with COPD have a history of asthma disease, and over 40% of patients with airflow limitation have ACO [6]. Eosinophil (EOS) is a common indicator to evaluate the level of airway EOS inflammation, which can guide the selection of stable drugs in COPD patients [7]. The main characteristic of asthma is eosinophilic airway inflammation. Serum EOS is a commonly used marker of eosinophilic airway inflammation, which can be used as a predictor of asthma severity and prognosis [8]. However, the value of serum EOS in the exacerbation risk and treatment guidance of COPD and asthma is still controversial, and currently, there is no serum EOS threshold for the diagnosis of COPD and asthma [9]. Therefore, this work reviewed the research progress of serum EOS in COPD and asthma, so as to offer some reference for the value of serum EOS in diagnosing and treating COPD and asthma.

1 Physiological and pathological characteristics of EOS

EOS is a kind of innate multifunctional immune cells, and the number of EOS in tissues is 100 times that in peripheral blood [10]. As an immune leukocyte, EOS accounts for less than 5% of total leukocytes (Figure 1). EOS is mainly formed in the bone marrow and enters tissues after staying in blood for about 25 h, but its duration in different tissues is uncertain [11]. Under normal circumstances, EOS is mainly distributed in the gastrointestinal tract and the thymus. When the body appears infection and other pathological states, a large amount of EOS will migrate to the lungs, promoting the abnormal release of inflammatory factors in the lung airway, resulting in inflammatory response. EOS can express immunoglobulin IgG, IgA, complement receptor, cytokine receptor, leukotriene (LT) receptor, prostate receptor, toll-like receptor, and other cell surface receptors [12,13,14]. The binding of these receptors to the embryo can stimulate the change of EOS activity and release lipid mediators and reactive oxygen species. The cell products of EOS [15,16] mainly include (1) a variety of positive particle proteins, basic proteins, and other granular media; (2) lipid mediators such as LT C4/FGE2/thrombus and platelet-activating factor (PAF); and (3) cytokines and chemokines of transforming growth factor β and interleukin (IL)-4, IL-5, IL-8, IL-10, and IL-12. The above EOS cell products participate in the occurrence and development of diseases by inhibiting airway cilia function, stimulating bronchoconstriction, promoting airway remodeling, and immune response.

Figure 1 Distribution of EOS in blood cells [17].
Figure 1

Distribution of EOS in blood cells [17].

Serum EOS is derived from bone marrow hematopoietic stem cells and has good short-term stability, which is affected by age, sex, baseline EOS level, and drug use [18]. Studies have shown that serum EOS levels in adults do not change with age but are susceptible to factors such as asthma, smoking, COPD, metabolic syndrome, and obesity, thus affecting serum EOS stability [19]. Serum EOS levels are associated with serum infections, dermatosis, allergic diseases, autoimmune diseases, myeloproliferative malignancies, pulmonary invasive hyper-EOS and EOS gastroenteritis [20], and serum EOS levels are also altered by simultaneous administration of drugs [21]. The influencing factors of EOS level change are shown in Figure 2. Serum EOS is highly variable [22], and its value in the diagnosis and treatment of respiratory diseases and clinical decision guidance remains to be further verified. EOS has a variety of functions, including cell synthesis and release of active substances, removal of harmful substances, tissue damage and repair, immune regulation, and other processes, as well as inhibiting tumor cell growth and promoting tumor cell apoptosis [23]. EOS mainly plays a role in host immune defense and post-parasitic immunity in allergic diseases, and there is a certain correlation between the amount of EOS and the clearance rate of viruses and pathogenic bacteria, suggesting that EOS has antibacterial properties [24]. In the lung, asthma is characterized by allergic reactions and Th2 lymphocyte-mediated eosinophilic inflammation. Acute exacerbation of COPD (AECOPD) exacerbation refers to exacerbation of airway inflammation in some AECOPD patients [25].

Figure 2 Influencing factors of EOS level change.
Figure 2

Influencing factors of EOS level change.

2 Research progress of serum EOS in COPD

2.1 Overview of COPD

COPD has become one of the common and frequently occurring diseases worldwide and is the fourth leading cause of human death worldwide. Relevant statistics show that in 2015, about 3.2 million people died due to COPD worldwide, an increase of 11.6% over 1990 [26]. The case fatality rate of COPD is increasing year by year and is expected to become the third leading cause of death in the world by 2030. China, as an agricultural country and a large population, currently has about 100 million people suffering from COPD. The prevalence rate of COPD in people over 40 years old is as high as 13.7%, and the incidence rate of COPD in rural people over 60 years old is more than 27% [1]. The main clinical manifestations of COPD are intermittent cough, sputum, shortness of breath or dyspnea, wheezing, chest tightness, chest congestion with loss of appetite, peripheral muscle atrophy and dysfunction, mental depression, and anxiety [27]. Current research results show that the occurrence of COPD is mainly influenced by genetic factors and environmental factors, and the genetic factors are mainly manifested in antitrypsin loss, and the proportion of COPD caused by antitrypsin loss is about 1.5% [28]. Environmental factors mainly include living area, altitude, age, smoking, dust exposure occupation, biofuel exposure, atmospheric smog, and respiratory tract infection (Figure 3). The incidence of COPD was positively correlated with age and inversely correlated with altitude. In stable COPD patients, under the stimulation of pathogen infection, improper diet, inhalation of allergens, and other inducing factors, the disease will be further aggravated and transformed into AECOPD. COPD can cause a series of complications, which not only affect lung function but also involve other organs outside the lung [29]. Therefore, timely and accurate diagnosis and evaluation of COPD and its severity have important guiding significance for the evaluation and treatment of COPD progression.

Figure 3 Risk factors of COPD.
Figure 3

Risk factors of COPD.

2.2 Pathogenesis of COPD and its relationship with EOS

Pathogenesis of COPD is still unclear. However, it is widely believed that the pathogenesis of COPD is related to airway inflammation, immune mechanism, oxidative stress imbalance, protease/antiprotease imbalance, emphysema overinflation, and inflation [30]. The specific pathogenesis of COPD is illustrated in Figure 4. At present, a large number of studies have pointed out that COPD is a chronic inflammatory development, in which a large number of neutrophils (NEU), macrophages, and T cells are involved, and its occurrence is correlated with the release of IL-8, LT B4, and other factors [31,32]. Studies have pointed out that stimulation of external factors (such as smoking) will cause B cells in the body to secrete a large amount of IgIC, which will aggravate the inflammatory response of the body [33]. On the other hand, CD8+ lymphocytes play an important role in the development of COPD. In terms of oxidative stress, inhaled particulate matter can produce oxidative free radicals, which can reduce the endogenous antioxidant products of the body, promote the oxidative stress reaction of the body, and aggravate the deterioration of lung function. The imbalance between excessive lipid peroxidation and antioxidant is closely related to COPD. In terms of protease/antiprotease imbalance, the content of protease in COPD patients is significantly increased, the increased protease causes pulmonary inflammatory infiltration, and fibroblasts produce a large number of factors such as NE and MMP, which further promotes the occurrence of emphysema, aggravates the inflammatory response, and promotes the severity of COPD. Lack of antiprotease will cause lung protease hydrolytic injury, resulting in chronic cell injury.

Figure 4 Pathogenesis of COPD [34].
Figure 4

Pathogenesis of COPD [34].

COPD exhibits obvious clinical heterogeneity. Most patients present with NEU inflammation, but some patients still present with increased EOS count. NEU are the main inflammatory cells of AECOPD, and bacterial infection can cause elevated NEU levels in the respiratory tract. At the same time, studies have found that EOS plays an important role in inflammation in 10–40% of COPD patients [35], suggesting that EOS may have a certain correlation with the occurrence and development of COPD. The differentiation and maturation process of EOS in the respiratory system is demonstrated in Figure 5. Stimulation of external factors (smoking, harmful substances) and viral infection can cause respiratory epithelial cells to release a large amount of thymic stromal lymphopoietin and IL-33, promote the change of IL-5 secretion, degranulate EOS, promote tissue damage, and aggravate inflammation. IL-5 is one of the main regulatory factors of EOS and is related to EOS production, release, migration, and survival. The level of IL-25 and IL-33 in lung tissue can affect the level of congenital non-T cells and thus regulate the up-regulation of IL-5 level and promote the increase of EOS level. Meanwhile, studies have shown that IL-33 can enhance Th2 cells, improve the survival rate of EOS, and induce superoxide anion production and degranulation of EOS [36]. Exogenous molecules such as nitric oxide and ozone would increase the expression level of EOS chemokines in airway epithelial cells, so that peripheral serum EOS could play a role in vascular endothelial cell adhesion and chemotaxis.

Figure 5 Differentiation and maturation of EOS [37].
Figure 5

Differentiation and maturation of EOS [37].

EOS participates in Th2 type immune response. Under the action of cytokines, EOS migrates to inflammatory tissues and releases a large number of cytokines, lipid mediators, and granulocins, among which granulocins are harmful to bronchial epithelium and closely related to airway inflammation [38]. In addition, activated EOS will release PAF, LTs, and other inflammatory mediators, causing bronchial contraction and mucosal microvascular leakage, and aggravating tissue damage. Bacterial or viral infections cause secretory IgA levels to rise, which activates EOS and releases eosinophilic positive ions and other proteins into body fluids, which increases airway mucus secretion, reduces ciliary movement, and leads to persistent airflow limitation in patients [39]. At the same time, it has been shown that the level of intercellular adhesion moleculin-1 increases during viral infection, which promotes the migration of EOS in the peripheral blood to the airway and aggravates airway inflammation [40,41]. Figure 6 demonstrates the incidence of COPD and its relationship with EOS.

Figure 6 The incidence of COPD and its relationship with EOS.
Figure 6

The incidence of COPD and its relationship with EOS.

2.3 Correlation between COPD clinical features and EOS

The subjects have been grouped based on serum EOS concentration differences [42,43]. Serum EOS levels greater than 200/μL or 2% significantly increased sputum EOS count and IgE, with obvious differences in age, sex, obesity, and smoking indices, and increased wheezing symptoms [44]. In addition, the score of Saint George’s respiratory questionnaire was increased, and the values of lung function indexes forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and FEV1/FVC were decreased remarkably. Serum EOS levels were negatively correlated with biochemical indices such as white blood cell, NEU%, and c-reactive protein. Patients with AECOPD with EOS levels below 2% had poorer lung function and were at higher risk for pneumonia, respiratory failure, and chronic pulmonary heart disease. At the same time, it has been reported that [45] clinical characteristics and lung function indices showed no great differences when serum EOS level was greater than 300/μL. Therefore, the correlation between the clinical characteristics of COPD and serum EOS remains controversial.

2.4 The relationship between diagnosis and treatment of COPD and EOS

There are few studies on the direct correlation between COPD diagnosis and EOS levels. In the Global Initiative for Chronic Obstructive Lung Disease scale, emphysema and NEU inflammation were more common in patients with grades B and D COPD. Chronic bronchitis is more common in patients with grades A and C COPD [8]. Induced sputum cell counting is the gold standard for evaluating airway EOS inflammation, but it is easy to be affected by subjective factors, difficult to take samples, and has certain limitations in clinical application. Serum EOS count is correlated with induced sputum cell count, but its correlation with COPD remains controversial. Some studies showed that serum EOS was correlated with induced sputum EOS, but the correlation was weak. The false positive rate of sputum EOS predicted by serum EOS was as high as 72.00% [46]. Ortega et al. [47] pointed out that serum EOS levels were significantly correlated with sputum EOS levels when serum EOS levels were lower than 210.6/μL but were susceptible to factors such as age and cardiovascular complications. Fractional exhaled nitric oxide (FENO) is a marker of inflammation in airway EOS with induced sputum cell count as the gold standard. Serum EOS and FENO levels both predicted the level of airway EOS inflammation, and serum EOS was superior, but serum EOS combined with FENO did not improve the diagnostic accuracy [48]. Serum EOS levels in COPD were monitored for 7 years [49] and showed great variability throughout the course of the disease. However, Negewo et al. [50] pointed out that serum EOS levels in COPD patients could be reasonably repeatable within 1 year. Therefore, the application value of serum EOS in the diagnosis of COPD needs further investigation.

The main inflammation was EOS. Currently, according to the different exacerbations of COPD, COPD is divided into mainly bacterial, mainly viral, mainly EOS, and a certain type of “oligo-immune” inflammation. According to different types of COPD diagnosis, the choice of treatment plan for patients can be guided. For COPD patients mainly with NEU, antibiotics can be used, and for COPD patients mainly with EOS, glucocorticoid can be used. Both clinical studies and Global Initiative for Chronic Obstructive Lung Disease concluded that serum EOS levels could guide the selection of glucocorticoid therapy in stable COPD. Studies have pointed out [51] that the mechanism of glucocorticoid in treating COPD, which is dominated by EOS, is mainly related to the regulation of EOS expression level by hormones. Hormones bind to the receptors on the nucleus and are transported to the nucleus to inhibit the synthesis of pro-inflammatory proteins and promote the apoptosis of EOS and other inflammatory cells, so as to achieve the purpose of treating COPD. An investigator [52] who administered hormone therapy to patients with COPD based on EOS found that lung function improved and hormone use was reduced by 49% after hormone therapy. Therefore, serum EOS is a potential biomarker for evaluating the efficacy of AECOPD. COPD patients with elevated serum EOS levels [53] responded to betamethasone/formoterol therapy. Patients with moderate-to-severe COPD treated with fluticasone/vilanterol had a lower incidence of AECOPD when serum EOS level was greater than 2%. There were also studies [54] that there was a bias in determining the treatment of COPD patients based on serum EOS levels.

2.5 Relationship between prognosis of COPD and EOS

The relationship between COPD prognosis and EOS mainly includes the following aspects. (1) Serum EOS reduction may be a marker of poor prognosis in COPD and was linked with increased mortality and length of hospital stay in patients with AECOPD. In addition, serum EOS reduction was also obviously linked with the duration of hospital stay, the need for mechanical ventilation, in-hospital death, and 30-day readmission and mortality in COPD patients. (2) Serum EOS increase was an independent predictor of AECOPD combined with pneumonia mortality. A retrospective analysis [55] of the correlation between serum EOS levels and length of ICU stay and mortality in COPD patients found that patients with serum EOS levels greater than 2% had significantly lower length of ICU stay and mortality than patients with serum EOS levels less than 2%. Barnes et al. [56] found that patients with AECOPD serum EOS ≥2% had lower CRP levels and significantly shortened hospital stay, suggesting that serum EOS level could be used as a biomarker for prognosis of COPD. Watz et al. [57] found that patients with serum EOS level greater than 2% had much shorter hospital stays than patients with serum EOS level less than 2% during the 1-year observation period, but there was no statistical difference in the rate of re-hospitalization and the time to first exacerbation. At the same time, there were no significant differences in respiratory symptoms, pulmonary function, and exacerbation rate in COPD patients with different serum EOS levels [58], suggesting that serum EOS levels could not be used as biomarkers of COPD phenotype. Therefore, the value of serum EOS levels in the prognosis of COPD needs further investigation.

3 Research progress of serum EOS in asthma

3.1 Overview of asthma

Asthma is a common and frequent disease in the respiratory department. With the aggravation of global air pollution, asthma incidence is increasing year by year in the time range, which is a global problem threatening human health. There are about 300 million asthma patients worldwide, and the incidence rate is 1–18% [59]. It is expected that the number of asthma patients worldwide will exceed 300 million by 2025. The asthma mortality rate is between 1.6 and 36.7 per 100,000, with the highest incidence among children. The asthma incidence of children aged 13–14 years is 0–30% [60]. There are about 30 million asthma patients in our country, accounting for 1/10 of the world’s asthma patients. The domestic asthma incidence is 0.5–5%, and the incidence of asthma in children aged 13–14 is 3–5% [61]. China has become one of the countries with a high asthma case fatality rate due to the factors of long-term poor control and untimely treatment. Therefore, it is of positive significance for human health to develop asthma prevention and control actively.

Asthma is mainly caused by both genetic and environmental factors. According to statistics, approximately 50.9% of asthma patients have a family history of allergies, and 37.5% of patients have a family history of asthma [62], suggesting that the occurrence of asthma may be related to gene regulation and immune regulation. Environmental factors mainly include external inhalants, infection, diet, climate, drugs, etc., external inhalants specific allergens (such as pollen, dust mites, fungi, and animal dander), and non-specific irritants (such as sulfuric acid, sulfur dioxide, formaldehyde, and formic acid) (Figure 7). After external inhalants enter the body, the airway mucosa will accumulate a large amount of external inhalants, promoting the occurrence of local or systemic immune response, and then leading to the occurrence of airway allergic inflammation [63]. When the body is infected with bacteria, viruses, mycoplasma, and other infectious sources will cause damage to the respiratory epithelium and promote the increase of respiratory responsiveness [64]. Long-term repeated infection is closely related to asthma occurrence. Diet is one of the factors that lead to asthma development in infants. Temperature, air pressure, humidity, strenuous exercise, drug use, and other factors are correlated with asthma development [65].

Figure 7 Environmental factors of asthma onset.
Figure 7

Environmental factors of asthma onset.

Asthma is a chronic airway inflammatory disease involving a variety of cells and cell components, which is clinically manifested by repeated wheezing, shortness of breath, chest tightness, cough, etc., which gets worse at night or early morning, most patients can be relieved by themselves or be relieved by treatment [66]. COPD patients have obvious airflow limitation, and their clinical symptoms are similar with little difference to asthma [67,68]. The differences in clinical and physiological characteristics between asthma and COPD are listed in Table 1.

Table 1

Clinical and physiological characteristics between asthma and COPD

COPD Asthma
Airway hyperreactivity Reactive with relatively lower responsiveness, less susceptible to stimuli Increased reactivity, easily triggered, leading to acute attacks
Etiology Factors such as smoking and prolonged exposure to air pollutants Caused by allergens, airway inflammation, and airway hyperresponsiveness
Airway inflammatory properties Chronic inflammation caused by NEU and macrophages Increased EOSs, inflammation mediated by T lymphocytes
Major inflammatory cell NEU EOS
Major lesion site Airway wall mucosal layer and deep tissue Airway wall mucosal layer
Airflow limiting mechanism Irreversible airway inflammation and structural damage Reversible airway spasms and increased airway mucus secretion
Airway obstruction Progressive aggravation, irreversible Changeable and reversible
Cell types of sputum Increased EOSs Increased EOSs
Cytokine IL-1β, IL-6, IL-8, and TNF-α IL-4, IL-5, IL-9, and IL-13
Inflammatory cell NEU and macrophages T lymphocytes and EOSs
Bronchiolar mucus cells Tissue metaplasia and hyperplasia Epithelial exfoliation
Pathological features Parenchymal cell destruction, emphysema, and massive mucus Parenchymal cells intact, no emphysema, and exudative mucus

3.2 The mechanism of asthma and its relationship with EOS

Asthma is a chronic inflammatory disease of the airway involving EOSs, mast cells, Th2, and other inflammatory cells, airway epithelial cells, and cell components. According to the classification and counting of sputum cells induced by airway inflammation indicators, asthma can be divided into eosinophilic, neutrophilic, mixed granulocyte, and oligoinflammatory cell types. Allergens are one of the main factors in the occurrence and development of asthma. The serum IgE level in asthma patients is elevated, which is one of the key links causing the occurrence and development of asthma. Chronic airway inflammation is the basis of asthma. The mechanism of asthma development mainly includes the following aspects [69–72]. (1) Allergy: after exposure to allergens, macrophages, lymphocytes, and granulocytes form antigen-presenting effect, which activates T lymphocytes and secretes a large amount of IL factors. Furthermore, B lymphocytes are regulated to increase IgE levels and adhere to mast cells, EOS, and basophil granulocytes, leading to chronic inflammatory pathological reactions in the body. When the body is exposed to allergens again, the release of inflammatory factors increases, promoting the occurrence of bronchial mucosal inflammation. (2) Airway inflammation: it is generally believed in current studies that asthma is related to the imbalance of Th1/Th2 ratio in the body. When the level of Th2 in the body is high, the expression of cytokines such as IL-4, IL-5, IL-6, and IL-13 will increase obviously. IL-4 can regulate IgE expression level and promote IgE-mediated humoral lymphatic response, resulting in asthma. IL-5 is mainly produced by mast cells, EOS, and TH2 cells. Massive secretion of IL-5 promotes the proliferation of EOS and migrates into the respiratory tract, causing airway epithelial cell damage and airway hyperresponse. The synergistic action of IL-4, IL-5, and IL-6 can stimulate the change of IgA secretion and mediate delayed asthma reaction. IL-13 may promote the synthesis of immunoglobulin IgE, which causes EOS to adhere to airway epithelial cells and trigger an inflammatory response. In addition, IL-13 promotes mucus secretion and participates in airway hyperresponsiveness. Some studies have shown that [73] the blood IL-10 content of asthma patients is significantly reduced, suggesting that IL-10 content is correlated with the occurrence and aggravation of airway inflammation. TNF-α is involved in the migration, adhesion, and infiltration of inflammatory cells, which is related to the occurrence of airway inflammation. (3) Airway hyperresponsiveness: when the airway is stimulated by sensitizing sources, it will cause chronic inflammation of the bronchial mucosa, expose the infected nerve endings of smooth muscle, cause premature and over-strong contraction and spasm of the airway, and eventually lead to asthma. (4) Airway remodeling: airway remodeling is the main pathological feature of asthma, which is mainly manifested by the damage and abnormal proliferation of airway smooth muscle cells. (5) Neuroregulatory mechanism: sensitizer stimulation can cause airway sensory nerve fibers to release peptide substance P, promote airway contraction, lead to airway mucus overreaction, cause inflammation in the body, and eventually lead to asthma. At present, there are few studies on the mechanism of neural regulation, and further studies are needed. (6) Emotional stimulation: studies have pointed out that emotional changes can stimulate cerebral cortex excitement, cause vagus nerve excitation, increase the release of acetylcholine in the body, and increase bronchial smooth muscle tension, leading to conditioned immune regulation. In addition, emotional stimulation will cause changes in the regulation of the endocrine system of the body through the hypothalamic–pituitary–adrenal axis, which will lead to changes in the release of inflammatory factors, increase of mucus secretion, decrease of ventilation ability, and ultimately lead to asthma [74]. The specific mechanism of asthma occurrence is displayed in Figure 8.

Figure 8 Mechanism of asthma occurrence.
Figure 8

Mechanism of asthma occurrence.

Th2-type immune response plays a key role in asthma development. Stimulation of allergens can increase the release of cytokines such as IL-4, IL-5, and IL-13 in Th2 cells in the body, promote the differentiation, recruitment, and activation of EOS in airway mucosa, further release a large number of inflammatory mediators, promote the occurrence of endogenous eosinophilic inflammatory reaction, and finally, cause asthma. Cytokines secreted by Th2 act together with CCL11 (eotaxin-1) to exert an important role in EOS recycling and allergic inflammation [75]. IL-4 and IL-13 can promote the expression of EOS chemokines, promote EOS adhesion and migration in the airway, increase the amount of EOS in the airway, and then secrete a large amount of granuloprotein, cytokines, and chemokines, leading to the damage of airway endothelial cells and mucous membranes, and eventually trigger asthma [76]. IL-5 is involved in the differentiation, maturation, and activation of EOS. EOS is a major inflammatory effector cell of asthma, involved in airway hyperreactivity, smooth muscle hypertrophy, and airway remodeling [77]. The relationship between asthma occurrence and EOS is illustrated in Figure 9. Studies have found that there is obvious eosinophilic inflammation in the airway sputum and blood of asthma patients in remission, to the extent that the thickness of the basement membrane is positively correlated with the eosinophilic inflammation of the airway wall.

Figure 9 Relationship between asthma occurrence and EOS.
Figure 9

Relationship between asthma occurrence and EOS.

3.3 Application of serum EOS in asthma evaluation

Tracheobronchial endoscopy, pulmonary function testing, and respiratory mucosal biopsy are commonly used methods for diagnosing and assessing asthma in clinical practice. Among these, pulmonary function testing might pose challenges for young children or patients with limited cognitive abilities. Asthma attacks are often transient, and if an attack does not coincide with the testing process, the results of pulmonary function testing might not capture the typical pathophysiological characteristics of the patient. Additionally, certain cases of early-stage or mild asthma might not exhibit clear airflow limitation [78], making pulmonary function testing unable to accurately detect these situations. Tracheobronchial endoscopy, being an invasive diagnostic technique, can cause discomfort and mild pain in patients and may lead to complications such as laryngospasm and bleeding [79]. It cannot comprehensively reflect dynamic changes in the airways and cannot provide quantitative data on lung function and airflow limitation. Respiratory mucosal biopsy involves invasive procedures, and therefore, many patients might be resistant to it. Sputum EOS is one of the commonly used methods to evaluate eosinophilic airway inflammation, and there is a significant correlation between sputum EOS and persistent airway inflammation, decreased lung function, and asthma severity [80]. Eosinophilic airway inflammation can be determined by bronchoalveolar lavage and increased EOS in induced sputum analysis. Several studies [81–83] have indicated that serum EOS is significantly correlated with sputum EOS, and serum EOS is a simple, safe, rapid, and potential marker of eosinophilic airway inflammation. A meta-analysis [84] showed that blood EOS level could better reflect the status of airway eosinophilic inflammation. It was found [85] that serum EOS percentage threshold of 2.7% could effectively predict eosinophilic airway inflammation. Castro et al. [86] showed that serum EOS percentage threshold of 3.0% could provide 78 and 91% sensitivity and specificity in predicting eosinophilic airway inflammation, respectively, suggesting that serum EOS could be a good substitute for sputum EOS. However, due to differences in research methods and severity of asthma patients, the optimal threshold value of serum EOS in asthma diagnosis is still controversial and needs to be further studied. FENO refers to the concentration of nitric oxide measured from exhaled gas at the end of expiration. Nitric oxide is primarily produced by airway epithelial cells and EOSs, and its levels are correlated with the degree of airway inflammation. In asthma patients, eosinophilic inflammation is a common type of inflammation, and FENO can serve as one of the representative indicators to assess airway inflammation. By measuring the FENO levels, it is possible to indirectly understand the extent of airway inflammation and conduct an assessment [87]. Elevated FENO levels are typically associated with increased eosinophilic inflammation, suggesting a potentially more severe degree of airway inflammation. Conversely, lower FENO levels may indicate relatively milder airway inflammation or a period of remission [88]. FENO cannot be used as a standalone method for diagnosing asthma, nor can it comprehensively evaluate the overall state of asthma control. It is usually employed in combination with a patient’s symptoms, clinical presentations, pulmonary function tests, and other auxiliary examination results to make comprehensive judgments and assessments.

3.4 Application of serum EOS in asthma severity and prognosis

Patients with eosinophilic asthma had lower lung function impairment, symptom control, and quality of life than those with non-eosinophilic asthma, and serum EOS count was significantly correlated with asthma severity. Therefore, some researchers pointed out that the increase in serum EOS count suggests that the decrease in lung function in asthma patients, and timely and effective treatment should be given [89]. Mallah et al. [90] investigated the correlation between serum EOS and lung function in asthma patients and found that serum EOS level was significantly negatively correlated with the value of FEV1, an indicator of lung function. Serum EOS level increased, which promoted airflow obstruction and further promoted lung function decline. Rupani and Teague [91] pointed out that serum EOS level was significantly positively correlated with the risk of asthma attack, and serum EOS count greater than 0.4 × 109/L suggested the progression of asthma attack or poor asthma control. Serum EOS counts [92] were associated with the severity of respiratory failure in acute asthma attacks, suggesting that serum EOS counts could be used to predict the risk of asthma deterioration when the EOS count was greater than 1.2 × 109/L. Simultaneous asthma patients may have a severe eosinophilic phenotype. These results suggest that serum EOS may be a potential asthma predictor biomarker.

4 Summary

This work examined the potential application value of serum EOS in patients with COPD and asthma pathogenesis, as well as the correlation between these two diseases. Serum EOS plays an important role in the pathogenesis, diagnosis, treatment, and prognosis of COPD and asthma and has potential clinical application. However, the assessment threshold still needs further study, which provides guidance for treating COPD and asthma in clinic.

  1. Funding information: Authors state no funding involved.

  2. Conflict of interest: Authors state no conflict of interest.

  3. Data availability statement: All data generated or analyzed during this study are included in this published article.

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Received: 2023-07-17
Revised: 2023-10-13
Accepted: 2023-10-30
Published Online: 2023-12-07

© 2023 the author(s), published by De Gruyter

This work is licensed under the Creative Commons Attribution 4.0 International License.

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  265. An advanced approach for fig leaf disease detection and classification: Leveraging image processing and enhanced support vector machine methodology
  266. Erratum
  267. Erratum to “Protein Z modulates the metastasis of lung adenocarcinoma cells”
  268. Erratum to “BRCA1 subcellular localization regulated by PI3K signaling pathway in triple-negative breast cancer MDA-MB-231 cells and hormone-sensitive T47D cells”
  269. Retraction
  270. Retraction to “Protocatechuic acid attenuates cerebral aneurysm formation and progression by inhibiting TNF-alpha/Nrf-2/NF-kB-mediated inflammatory mechanisms in experimental rats”
https://doi.org/10.1515/biol-2022-0779
Keywords for this article
eosinophil; chronic obstructive pulmonary disease; asthma; pathogenesis; diagnosis; prognosis
Creative Commons
BY 4.0

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  126. Clinicopathological features and differential diagnosis of gastric pleomorphic giant cell carcinoma
  127. Traumatic brain injury and rTMS-ERPs: Case report and literature review
  128. Extracellular fibrin promotes non-small cell lung cancer progression through integrin β1/PTEN/AKT signaling
  129. Knockdown of DLK4 inhibits non-small cell lung cancer tumor growth by downregulating CKS2
  130. The co-expression pattern of VEGFR-2 with indicators related to proliferation, apoptosis, and differentiation of anagen hair follicles
  131. Inflammation-related signaling pathways in tendinopathy
  132. CD4+ T cell count in HIV/TB co-infection and co-occurrence with HL: Case report and literature review
  133. Clinical analysis of severe Chlamydia psittaci pneumonia: Case series study
  134. Bioinformatics analysis to identify potential biomarkers for the pulmonary artery hypertension associated with the basement membrane
  135. Influence of MTHFR polymorphism, alone or in combination with smoking and alcohol consumption, on cancer susceptibility
  136. Catharanthus roseus (L.) G. Don counteracts the ampicillin resistance in multiple antibiotic-resistant Staphylococcus aureus by downregulation of PBP2a synthesis
  137. Combination of a bronchogenic cyst in the thoracic spinal canal with chronic myelocytic leukemia
  138. Bacterial lipoprotein plays an important role in the macrophage autophagy and apoptosis induced by Salmonella typhimurium and Staphylococcus aureus
  139. TCL1A+ B cells predict prognosis in triple-negative breast cancer through integrative analysis of single-cell and bulk transcriptomic data
  140. Ezrin promotes esophageal squamous cell carcinoma progression via the Hippo signaling pathway
  141. Ferroptosis: A potential target of macrophages in plaque vulnerability
  142. Predicting pediatric Crohn's disease based on six mRNA-constructed risk signature using comprehensive bioinformatic approaches
  143. Applications of genetic code expansion and photosensitive UAAs in studying membrane proteins
  144. HK2 contributes to the proliferation, migration, and invasion of diffuse large B-cell lymphoma cells by enhancing the ERK1/2 signaling pathway
  145. IL-17 in osteoarthritis: A narrative review
  146. Circadian cycle and neuroinflammation
  147. Probiotic management and inflammatory factors as a novel treatment in cirrhosis: A systematic review and meta-analysis
  148. Hemorrhagic meningioma with pulmonary metastasis: Case report and literature review
  149. SPOP regulates the expression profiles and alternative splicing events in human hepatocytes
  150. Knockdown of SETD5 inhibited glycolysis and tumor growth in gastric cancer cells by down-regulating Akt signaling pathway
  151. PTX3 promotes IVIG resistance-induced endothelial injury in Kawasaki disease by regulating the NF-κB pathway
  152. Pancreatic ectopic thyroid tissue: A case report and analysis of literature
  153. The prognostic impact of body mass index on female breast cancer patients in underdeveloped regions of northern China differs by menopause status and tumor molecular subtype
  154. Report on a case of liver-originating malignant melanoma of unknown primary
  155. Case report: Herbal treatment of neutropenic enterocolitis after chemotherapy for breast cancer
  156. The fibroblast growth factor–Klotho axis at molecular level
  157. Characterization of amiodarone action on currents in hERG-T618 gain-of-function mutations
  158. A case report of diagnosis and dynamic monitoring of Listeria monocytogenes meningitis with NGS
  159. Effect of autologous platelet-rich plasma on new bone formation and viability of a Marburg bone graft
  160. Small breast epithelial mucin as a useful prognostic marker for breast cancer patients
  161. Continuous non-adherent culture promotes transdifferentiation of human adipose-derived stem cells into retinal lineage
  162. Nrf3 alleviates oxidative stress and promotes the survival of colon cancer cells by activating AKT/BCL-2 signal pathway
  163. Favorable response to surufatinib in a patient with necrolytic migratory erythema: A case report
  164. Case report of atypical undernutrition of hypoproteinemia type
  165. Down-regulation of COL1A1 inhibits tumor-associated fibroblast activation and mediates matrix remodeling in the tumor microenvironment of breast cancer
  166. Sarcoma protein kinase inhibition alleviates liver fibrosis by promoting hepatic stellate cells ferroptosis
  167. Research progress of serum eosinophil in chronic obstructive pulmonary disease and asthma
  168. Clinicopathological characteristics of co-existing or mixed colorectal cancer and neuroendocrine tumor: Report of five cases
  169. Role of menopausal hormone therapy in the prevention of postmenopausal osteoporosis
  170. Precisional detection of lymph node metastasis using tFCM in colorectal cancer
  171. Advances in diagnosis and treatment of perimenopausal syndrome
  172. A study of forensic genetics: ITO index distribution and kinship judgment between two individuals
  173. Acute lupus pneumonitis resembling miliary tuberculosis: A case-based review
  174. Plasma levels of CD36 and glutathione as biomarkers for ruptured intracranial aneurysm
  175. Fractalkine modulates pulmonary angiogenesis and tube formation by modulating CX3CR1 and growth factors in PVECs
  176. Novel risk prediction models for deep vein thrombosis after thoracotomy and thoracoscopic lung cancer resections, involving coagulation and immune function
  177. Exploring the diagnostic markers of essential tremor: A study based on machine learning algorithms
  178. Evaluation of effects of small-incision approach treatment on proximal tibia fracture by deep learning algorithm-based magnetic resonance imaging
  179. An online diagnosis method for cancer lesions based on intelligent imaging analysis
  180. Medical imaging in rheumatoid arthritis: A review on deep learning approach
  181. Predictive analytics in smart healthcare for child mortality prediction using a machine learning approach
  182. Utility of neutrophil–lymphocyte ratio and platelet–lymphocyte ratio in predicting acute-on-chronic liver failure survival
  183. A biomedical decision support system for meta-analysis of bilateral upper-limb training in stroke patients with hemiplegia
  184. TNF-α and IL-8 levels are positively correlated with hypobaric hypoxic pulmonary hypertension and pulmonary vascular remodeling in rats
  185. Stochastic gradient descent optimisation for convolutional neural network for medical image segmentation
  186. Comparison of the prognostic value of four different critical illness scores in patients with sepsis-induced coagulopathy
  187. Application and teaching of computer molecular simulation embedded technology and artificial intelligence in drug research and development
  188. Hepatobiliary surgery based on intelligent image segmentation technology
  189. Value of brain injury-related indicators based on neural network in the diagnosis of neonatal hypoxic-ischemic encephalopathy
  190. Analysis of early diagnosis methods for asymmetric dementia in brain MR images based on genetic medical technology
  191. Early diagnosis for the onset of peri-implantitis based on artificial neural network
  192. Clinical significance of the detection of serum IgG4 and IgG4/IgG ratio in patients with thyroid-associated ophthalmopathy
  193. Forecast of pain degree of lumbar disc herniation based on back propagation neural network
  194. SPA-UNet: A liver tumor segmentation network based on fused multi-scale features
  195. Systematic evaluation of clinical efficacy of CYP1B1 gene polymorphism in EGFR mutant non-small cell lung cancer observed by medical image
  196. Rehabilitation effect of intelligent rehabilitation training system on hemiplegic limb spasms after stroke
  197. A novel approach for minimising anti-aliasing effects in EEG data acquisition
  198. ErbB4 promotes M2 activation of macrophages in idiopathic pulmonary fibrosis
  199. Clinical role of CYP1B1 gene polymorphism in prediction of postoperative chemotherapy efficacy in NSCLC based on individualized health model
  200. Lung nodule segmentation via semi-residual multi-resolution neural networks
  201. Evaluation of brain nerve function in ICU patients with Delirium by deep learning algorithm-based resting state MRI
  202. A data mining technique for detecting malignant mesothelioma cancer using multiple regression analysis
  203. Markov model combined with MR diffusion tensor imaging for predicting the onset of Alzheimer’s disease
  204. Effectiveness of the treatment of depression associated with cancer and neuroimaging changes in depression-related brain regions in patients treated with the mediator-deuterium acupuncture method
  205. Molecular mechanism of colorectal cancer and screening of molecular markers based on bioinformatics analysis
  206. Monitoring and evaluation of anesthesia depth status data based on neuroscience
  207. Exploring the conformational dynamics and thermodynamics of EGFR S768I and G719X + S768I mutations in non-small cell lung cancer: An in silico approaches
  208. Optimised feature selection-driven convolutional neural network using gray level co-occurrence matrix for detection of cervical cancer
  209. Incidence of different pressure patterns of spinal cerebellar ataxia and analysis of imaging and genetic diagnosis
  210. Pathogenic bacteria and treatment resistance in older cardiovascular disease patients with lung infection and risk prediction model
  211. Adoption value of support vector machine algorithm-based computed tomography imaging in the diagnosis of secondary pulmonary fungal infections in patients with malignant hematological disorders
  212. From slides to insights: Harnessing deep learning for prognostic survival prediction in human colorectal cancer histology
  213. Ecology and Environmental Science
  214. Monitoring of hourly carbon dioxide concentration under different land use types in arid ecosystem
  215. Comparing the differences of prokaryotic microbial community between pit walls and bottom from Chinese liquor revealed by 16S rRNA gene sequencing
  216. Effects of cadmium stress on fruits germination and growth of two herbage species
  217. Bamboo charcoal affects soil properties and bacterial community in tea plantations
  218. Optimization of biogas potential using kinetic models, response surface methodology, and instrumental evidence for biodegradation of tannery fleshings during anaerobic digestion
  219. Understory vegetation diversity patterns of Platycladus orientalis and Pinus elliottii communities in Central and Southern China
  220. Studies on macrofungi diversity and discovery of new species of Abortiporus from Baotianman World Biosphere Reserve
  221. Food Science
  222. Effect of berrycactus fruit (Myrtillocactus geometrizans) on glutamate, glutamine, and GABA levels in the frontal cortex of rats fed with a high-fat diet
  223. Guesstimate of thymoquinone diversity in Nigella sativa L. genotypes and elite varieties collected from Indian states using HPTLC technique
  224. Analysis of bacterial community structure of Fuzhuan tea with different processing techniques
  225. Untargeted metabolomics reveals sour jujube kernel benefiting the nutritional value and flavor of Morchella esculenta
  226. Mycobiota in Slovak wine grapes: A case study from the small Carpathians wine region
  227. Elemental analysis of Fadogia ancylantha leaves used as a nutraceutical in Mashonaland West Province, Zimbabwe
  228. Microbiological transglutaminase: Biotechnological application in the food industry
  229. Influence of solvent-free extraction of fish oil from catfish (Clarias magur) heads using a Taguchi orthogonal array design: A qualitative and quantitative approach
  230. Chromatographic analysis of the chemical composition and anticancer activities of Curcuma longa extract cultivated in Palestine
  231. The potential for the use of leghemoglobin and plant ferritin as sources of iron
  232. Investigating the association between dietary patterns and glycemic control among children and adolescents with T1DM
  233. Bioengineering and Biotechnology
  234. Biocompatibility and osteointegration capability of β-TCP manufactured by stereolithography 3D printing: In vitro study
  235. Clinical characteristics and the prognosis of diabetic foot in Tibet: A single center, retrospective study
  236. Agriculture
  237. Biofertilizer and NPSB fertilizer application effects on nodulation and productivity of common bean (Phaseolus vulgaris L.) at Sodo Zuria, Southern Ethiopia
  238. On correlation between canopy vegetation and growth indexes of maize varieties with different nitrogen efficiencies
  239. Exopolysaccharides from Pseudomonas tolaasii inhibit the growth of Pleurotus ostreatus mycelia
  240. A transcriptomic evaluation of the mechanism of programmed cell death of the replaceable bud in Chinese chestnut
  241. Melatonin enhances salt tolerance in sorghum by modulating photosynthetic performance, osmoregulation, antioxidant defense, and ion homeostasis
  242. Effects of plant density on alfalfa (Medicago sativa L.) seed yield in western Heilongjiang areas
  243. Identification of rice leaf diseases and deficiency disorders using a novel DeepBatch technique
  244. Artificial intelligence and internet of things oriented sustainable precision farming: Towards modern agriculture
  245. Animal Sciences
  246. Effect of ketogenic diet on exercise tolerance and transcriptome of gastrocnemius in mice
  247. Combined analysis of mRNA–miRNA from testis tissue in Tibetan sheep with different FecB genotypes
  248. Isolation, identification, and drug resistance of a partially isolated bacterium from the gill of Siniperca chuatsi
  249. Tracking behavioral changes of confined sows from the first mating to the third parity
  250. The sequencing of the key genes and end products in the TLR4 signaling pathway from the kidney of Rana dybowskii exposed to Aeromonas hydrophila
  251. Development of a new candidate vaccine against piglet diarrhea caused by Escherichia coli
  252. Plant Sciences
  253. Crown and diameter structure of pure Pinus massoniana Lamb. forest in Hunan province, China
  254. Genetic evaluation and germplasm identification analysis on ITS2, trnL-F, and psbA-trnH of alfalfa varieties germplasm resources
  255. Tissue culture and rapid propagation technology for Gentiana rhodantha
  256. Effects of cadmium on the synthesis of active ingredients in Salvia miltiorrhiza
  257. Cloning and expression analysis of VrNAC13 gene in mung bean
  258. Chlorate-induced molecular floral transition revealed by transcriptomes
  259. Effects of warming and drought on growth and development of soybean in Hailun region
  260. Effects of different light conditions on transient expression and biomass in Nicotiana benthamiana leaves
  261. Comparative analysis of the rhizosphere microbiome and medicinally active ingredients of Atractylodes lancea from different geographical origins
  262. Distinguish Dianthus species or varieties based on chloroplast genomes
  263. Comparative transcriptomes reveal molecular mechanisms of apple blossoms of different tolerance genotypes to chilling injury
  264. Study on fresh processing key technology and quality influence of Cut Ophiopogonis Radix based on multi-index evaluation
  265. An advanced approach for fig leaf disease detection and classification: Leveraging image processing and enhanced support vector machine methodology
  266. Erratum
  267. Erratum to “Protein Z modulates the metastasis of lung adenocarcinoma cells”
  268. Erratum to “BRCA1 subcellular localization regulated by PI3K signaling pathway in triple-negative breast cancer MDA-MB-231 cells and hormone-sensitive T47D cells”
  269. Retraction
  270. Retraction to “Protocatechuic acid attenuates cerebral aneurysm formation and progression by inhibiting TNF-alpha/Nrf-2/NF-kB-mediated inflammatory mechanisms in experimental rats”
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