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Chen, Y.; Chang, Y.; , .; Hsiao, C.; Lin, M. Potential Biomarkers for Asthma and COPD Overlap. Encyclopedia. Available online: (accessed on 20 June 2024).
Chen Y, Chang Y,  , Hsiao C, Lin M. Potential Biomarkers for Asthma and COPD Overlap. Encyclopedia. Available at: Accessed June 20, 2024.
Chen, Yung-Che, Yu-Ping Chang,  , Chang-Chun Hsiao, Meng-Chih Lin. "Potential Biomarkers for Asthma and COPD Overlap" Encyclopedia, (accessed June 20, 2024).
Chen, Y., Chang, Y., , ., Hsiao, C., & Lin, M. (2022, June 03). Potential Biomarkers for Asthma and COPD Overlap. In Encyclopedia.
Chen, Yung-Che, et al. "Potential Biomarkers for Asthma and COPD Overlap." Encyclopedia. Web. 03 June, 2022.
Potential Biomarkers for Asthma and COPD Overlap

Asthma and COPD overlap (ACO) is characterized by patients presenting with persistent airflow limitation and features of both asthma and COPD. It is associated with a higher frequency and severity of exacerbations, a faster lung function decline, and a higher healthcare cost.  ACO-related biomarkers can be classified into four categories: neutrophil-mediated inflammation, Th2 cell responses, arachidonic acid-eicosanoids pathway, and metabolites.

asthma-chronic obstructive pulmonary disease overlap epigenetics

1. Introduction

1.1. Asthma and Chronic Obstructive Pulmonary Disease Overlap Is Associated with Higher Frequency and Severity of Exacerbations and Higher Health Care Cost

Asthma and chronic obstructive pulmonary disease (COPD) are the two most common obstructive airway diseases. Asthma and COPD overlap (ACO) is characterized by patients presenting with persistent airflow limitation and features of both asthma and COPD. A recent meta-analysis demonstrates a high symptom burden, including dyspnea and wheezing, a lower lung function, and a higher frequency and severity of exacerbations associated with ACO compared with simple asthma and COPD [1]. Patients with ACO have increased disease severity, live a poorer quality of life, and incur higher healthcare costs when compared with patients with asthma or COPD alone [2][3]. The frequency of ACO-related hospitalization increases, the medical utilization rate increases, and the survival time is shortened compared with simple asthma and COPD [4][5]. Patients with ACO based on late onset asthma had the most rapid decline in lung function with a forced expiration volume at 1 s (FEV1) decline of 49.6 mL/year, compared with 39.5 mL/year in COPD alone, 34.5 mL/year in asthma alone, and 27.3 mL/year in ACO patients based on early onset asthma [6][7][8][9]. Patients with ACO had higher respiratory resistance and reactance during tidal breathing, but a smaller gap between the inspiratory and expiratory phases, compared with simple COPD [10]. ACO also had increased bronchial wall thickening, increased airway remodeling, and increased airway hyper-responsiveness compared with asthma and COPD patients [11][12]. ACO likely encompasses a wide spectrum of phenotypes, e.g., COPD with eosinophilia and partially reversible airflow limitation, severe asthma with neutrophilia and fixed airflow limitation, or elderly non-smokers with long-standing asthma and irreversible airflow limitation [3][4][13]. Although there is no universally accepted definition of ACO at present, it is recommended that ACO be defined based on the presence of persistent airflow limitation (post-bronchodilator FEV1/forced vital capacity (FVC) ratio < 70%) in symptomatic individuals 40 years of age and older, a well-documented history of asthma, probably before 40 years of age, and a significant exposure history to cigarette or biomass smoke, accompanied by one of the hyper-responsive features, including atopy, allergic rhinitis, eosinophilia, and positive bronchodilator response [14]. The global burdens of asthma and chronic obstructive pulmonary disease (COPD) are increasing. Each of which was estimated to affect approximately 339 million and 251 million people worldwide in 2016, while ACO may represent around 29.6% of COPD patients and around 26.5% of asthma patients [13].

1.2. Systemic Inflammation in COPD and Asthma Is Driven by Th1 and Th2 Immune Responses, Respectively, while Both Immune Responses May Contribute to Airway Remodeling in ACO

Asthma is usually characterized by airway hyper-responsiveness, leading to reversible airflow obstruction based on type 2 inflammation with eosinophilia. In contrast, COPD shows progressive and irreversible airflow obstruction, typically caused by smoking or biomass, and is associated with neutrophilic inflammation involving CD4/CD8 T lymphocytes and macrophages. Systemic inflammation is a feature of both COPD and asthma, and contributes to airway remodeling, airflow limitation, and subsequent symptoms. Inflammation in COPD is typically driven by T-helper (Th) 1 immune responses, which enhance cell-mediated immunity and phagocyte-dependent inflammation through the production of interleukin (IL)-2, IL6, IL-8, IL-9, IL-17A, interferon-γ, and tumor necrosis factor (TNF)-α [15][16]. Pro-inflammatory cells, such as dendritic cells, neutrophils, and macrophages, are recruited to small airways and functionally altered by oxidative stress, intracellular activation of the transcription factor nuclear factor-κB (NF-κB), and defective bacterial phagocytosis, resulting in airflow limitation [16][17]. Key players of inflammatory response in asthma are Th2 and type 2 innate lymphoid cells, which produce IL-4, IL-5, IL-6, IL-9, IL-13, and IL-17E, resulting in overt immunoglobulin E (IgE) production, eosinophil accumulation, and inhibition of phagocyte-independent inflammation [15][17][18]. The two different inflammatory mechanisms involved in asthma and COPD may overlap in ACO patients. Studies have shown that ACO patients have higher fractions of exhaled nitric oxide (FeNO), higher blood eosinophil counts and percentages, and higher Th2 inflammation markers than COPD patients, as well as increased total and specific IgE levels [2][13][19][20]. However, similarities and differences between specific gene expression profiles in ACO, asthma, and COPD have not yet been studied, but could add to the understanding of the biology underlying the clinical and pathologic overlap between asthma and COPD.

2. Potential Biomarkers for ACO

Table 1 lists important molecules and their roles in the pathology and clinical phenotypes of ACO.
Table 1. Important molecules and their roles in the pathology and clinical phenotypes of asthma and chronic obstructive pulmonary disease overlap (ACO).

2.1. Neutrophilic Inflammation-Related

TNF-α regulates inflammatory cell functions such as cell proliferation, survival, differentiation, and apoptosis, and its genetic variant TNF-α-308 GA contributes to the susceptibility to COPD. Blood TNF-α concentrations of ACO patients were higher than that of asthmatics, but lower than that of pure COPD patients [25][26]. On the other hand, TNF-α was up-regulated in ACO mice versus either COPD or asthma mice [27]. As an anti-inflammatory cytokine, IL-10 has the capacity to suppress excessive inflammation by increasing M2 polarization and decreasing neutrophil infiltration. IL10 was down-regulated in ACO patients versus COPD [26]. Likewise, cathelicidin antimicrobial peptide (CAMP; LL37) was down-regulated in ACO patients versus COPD, while it not only directly recruits immunocompetent cells but also inhibits pro-inflammatory cytokine synthesis [35].
Neutrophil gelatinase-associated lipocalin (NGAL) is abundantly secreted by neutrophils and other immune cells during bacterial infections to hamper bacterial growth through restriction of iron availability and contributes to activation of iron-responsive genes like ferritin and transferrin receptors. NGAL protein levels have been shown to be elevated in sputum or serum samples from ACO patients versus COPD or asthma [21]. Given that NGAL has been demonstrated to be a good marker for early diagnosis of acute kidney injury and the prognosis of colon and breast cancers, it is less practicable to use this single marker to discriminate ACO from COPD or asthma [36].
Spleen associated tyrosine kinase (SYK), a 72kD non-receptor protein tyrosine kinase, can trigger cell degranulation and histamine release in human basophils through FcεRI-mediated signaling pathways and is required for neutrophils to form neutrophil extracellular traps. Phosphorylated SYK binds to the ITAM, triggering its downstream inflammatory signal cascades, including NF-κB and NLRP3, while the specific SYK inhibitor, EAPP-2, significantly down-regulates the expression of NF-κB, phosphorylated-NF-κB, and NLRP3 in ACO mice and in LPS-induced RAW264.7 macrophages in vitro [29].

2.2. Th2 Response-Related

In an allergic inflammatory microenvironment, pro-inflammatory cytokines and oxidative stress might up regulate the production of nitric oxide (NO) synthetase-2-derived NO, which produces strong oxidizing reactive nitrogen species, such as peroxynitrite, leading to cell damage in the airways [37]. IgE is synthesized by lymphocytes B upon IL-4-induced Ig class switching, and causes allergic inflammation process through interacting with dendritic cells, mast cells, eosinophils, airway epithelial cells and airway smooth muscle cells [20]. Periostin is produced by airway epithelial cells in response to type2 cytokines IL4 and IL13 stimuli, and augments eosinophilic inflammation through the αMβ2 integrin and the generation of a superoxide anion [31]. IL5 promotes recruitment and survival of eosinophils in airways as well as maturation of granules and contributes to bronchoconstriction, allergic response, fibrosis, epithelial injury, and oxidative stress. Fractional exhaled NO (FENO), IgE, serum periostin, and serum IL5, which are typical biomarkers of Th2 or eosinophilic responses, have all been reported to be able to distinguish ACO from COPD [30][31][34][38]. There are some differences in Th2 signatures between the two main types of ACO. Asthmatic smokers with chronic airflow obstruction (post-bronchodilator FEV1/FVC ≤ 0.7) had higher blood eosinophil counts than but similar FENO to simple COPD patients, while COPD patients with eosinophilia (≥200 eosinophils·μL−1) had higher FENO and blood eosinophil counts than both asthmatic smoker with chronic airflow obstruction and simple COPD patients [39].TBX21 and GATA3 have conventionally been regarded as a transcription factor that drives the differentiation of Th1 and Th2 cells, respectively, and increased TBX21/GATA3 gene expression ratios were found in ACO patients versus COPD or asthma [32][40]. IL-6 is a pleotropic cytokine produced in response to tissue damage, and might favor Th2 and Th17 polarization by stimulating STAT3 [41]. IL-6 was up-regulated in both ACO patients and ACO mice versus COPD or asthma [26][27]. IL-17E also induces allergic inflammation in favor of Th2 immune response. IL-17E was up-regulated in ACO patients versus COPD [26][42].
Eosinophil-derived neurotoxin (EDN) is one of the four specific granules of the human eosinophilic leukocyte and is released when these cells are activated by Th2 cytokines. EDN has been determined to be a specific biomarker in eosinophil-associated pathophysiologies, including asthma exacerbations, cow’s milk allergy, and eosinophilic esophagitis [43]. Recently, serum EDN was found to be higher in ACO patients than that in asthma or COPD patients and had the highest specificity (82.4%) when combined with high serum YKL-40 levels based on cutoff values derived by receiver operating characteristics analysis (EDN: 23.0 ng/mL; YKL-40: 61.3 ng/mL) [22].

2.3. Arachidonic Acid-Eicosanoid Pathway-Related

Arachidonic acid is an essential unsaturated fatty acid and is metabolized to eicosanoids and bioactive lipid mediators, which augment type 2 inflammatory responses in the airway, including potent bronchoconstriction, recruiting, and activating T cells, eosinophils, and antigen presenting cells, promoting the secretion of mucus, promoting the proliferation of human airway epithelial cells and smooth muscle cells, and increasing collagen deposition. Several eicosanoids metabolized through lipoxygenase, including TETE, HPETE, and HPODE, in serum have been shown to be able to distinguish ACO from COPD [33]. Prostaglandin D2 synthase (PGD2) has been reported to be higher in asthma and ACO patients than in COPD patients [34].

2.4. Metabolites-Related

Metabolites are produced during normal endogenous metabolism within biofluids, cells, tissues, or organisms, and the ever-expanding metabolomics approach has provided new insight into mechanistic changes associated with various diseases. Five serum metabolites, including L-serine, L-threonine, ethanolamine, D-mannose, and succinic acid, were found to be significantly decreased in ACO as compared with asthma and COPD patients, providing new insights into the altered pathways which could be contributing to the higher mortality and morbidity in ACO [26]. Another 12 metabolites, including lipid, isoleucine, N-acetylglycoproteins, valine, glutamate, citric acid, glucose, L-leucine, lysine, asparagine, phenylalanine, and histidine, were dysregulated in ACO patients when compared with both asthma and COPD [44]. Isopropanol and acetone were increased in exhaled breath condensate from ACO patients versus COPD or asthma, while valine was decreased [45]. Many study groups have reported altered expressions of various metabolites in respiratory diseases, so it is an emerging research area with a large potential for developing novel biomarkers. However, the underlying mechanisms by which these metabolites correlate with neutrophil-mediated inflammation or Th2 responses in ACO require further investigation.


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