Comprehensive analysis of allergen-specific IgE in COPD: mite-specific IgE specifically related to the diagnosis of asthma-COPD overlap

Abstract

Background Although the relationship between allergic sensitization and increased respiratory symptoms of chronic obstructive pulmonary disease (COPD) has been suggested, which allergen has a significant effect on COPD pathology is unclear. This study aimed to identify the specific IgE related to clinical features of COPD and the diagnosis of asthma-COPD overlap (ACO). Methods We recruited 76 patients with COPD and analyzed 39 IgE using panel IgE test (View Allergy 39®). ACO was diagnosed according to the Japanese Respiratory Society Guidelines. Results As for perennial aeroallergens, the positivity for moth (31.5%), Candida (23.7%), Dermatophagoides pteronyssinus (22.4%) and house dust (22.4%), and concerning pollen, Japanese cedar (35.5%) and Japanese cypress (22.2%) exceeded 20%. Only the positivity of IgE for Dermatophagoides pteronyssinus and house dust was significantly higher in ACO compared with that in non-ACO COPD. Moreover, it contributed to the diagnosis of ACO in an IgE class-dependent manner. Patients with cockroach IgE exhibited higher residual volume, whereas those with Japanese cedar IgE exhibited better diffusion capacity than negative patients. The contribution for ACO diagnosis by the receiver operating characteristic curve analysis was comparable among total IgE (cutoff value: 158 IU/mL), blood eosinophil count (234/μL), and fraction of exhaled nitric oxide (31.0 ppb). Conclusions The prominent role of mite-specific IgE in the diagnosis and pathology of ACO and the potentially detrimental effect of cockroach sensitization on air trapping in COPD were suggested. The finding highlights the future development of a treatment targeting IgE as a treatable trait in COPD.

Real-World Status of Medical Care and Treatment of Chronic Obstructive Pulmonary Disease by Respiratory Specialists in Japan

“…In contrast, other studies evaluating the proportions of patients in whom examinations and tests were implemented according to the ACO diagnostic criteria were mainly single-center studies. These studies, however, reported higher proportions of patients with the data necessary for ACO diagnosis than the proportions observed in the present study [13][14][15]. A single-center study retrospectively confirmed that the proportion of patients with the data necessary for ACO diagnosis was 66.9% (111/166 patients), including 23 patients who had test results for all ACO diagnostic items [13].…”

Relationship between allergic transfusion reactions and allergic predisposition among pediatric patients with hematological/oncological disease

“…Patients were stratified according to the total IgE level; an IgE level > 360 IU/mL was indicated as the reference standard range of the measurement kit (IATRO‐ACE IgE II, LSI Medience Corporation, Tokyo, Japan). Allergen‐specific IgE levels were analyzed using a panel IgE test (View Allergy 39®, Thermo Fisher Diagnostics K.K., Tokyo, Japan) 22,23 . The results of each allergen‐specific IgE, analyzed with View Allergy 39®, were classified into seven stages from classes 0 to 6.…”

“…Allergen-specific IgE levels were analyzed using a panel IgE test (View Allergy 39 ® , Thermo Fisher Diagnostics K.K., Tokyo, Japan). 22,23 The results of each allergen-specific IgE, analyzed with View Allergy 39 ® , were classified into seven stages from classes 0 to 6. An index value of <0.27 was considered to be negative and categorized in class 0; values between 0.27 and 0.50 were considered to be false-positive and categorized in class 1; and index values of ≥0.50 were considered to be positive; values of ≥0.…”

Unraveling the Pathogenesis of Asthma and Chronic Obstructive Pulmonary Disease Overlap: Focusing on Epigenetic Mechanisms

“…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 [ 28 ]. 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 [ 29 ].…”

“…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 our understanding of the biology underlying the clinical and pathologic overlap between asthma and COPD.…”