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Published on: May 30, 2020
Morphological and molecular characteristics of "difficult" asthma
Polina A Selivanova1, Evgeny S Kulikov, Olga V Kozina
1Department of Therapy, Siberian State Medical University, Tomsk 634050, Russian Federation. p.selivanova@mail.ru
Summary
Severe asthma variants like brittle asthma and persistent airflow limitation show distinct cellular and molecular differences. Understanding these variations is key to developing targeted treatments for difficult-to-treat asthma.
Area of Science:
- Pulmonary Medicine
- Immunology
- Genetics
Background:
- Severe asthma presents with clinical variants including persistent airflow limitation and brittle asthma.
- Pathogenetic mechanisms underlying these asthma subtypes remain poorly understood.
- Differentiating severe asthma subtypes is crucial for effective treatment strategies.
Purpose of the Study:
- To compare the morphological and molecular features of brittle asthma and asthma with persistent airflow limitation against mild-to-moderate asthma.
- To analyze cellular structure and gene expression in bronchial mucosa of different asthma phenotypes.
- To elucidate the underlying mechanisms of severe asthma heterogeneity.
Main Methods:
- Bronchoscopic evaluation of 42 asthma patients: 10 brittle asthma, 10 persistent airflow limitation, 22 mild-to-moderate asthma.
- Morphometric and cytological analysis of bronchial mucosa.
- Quantitative real-time PCR to measure mRNA levels of ADRB2, HRH1, and CHRM3 genes.
Main Results:
- Mild-to-moderate asthma showed higher eosinophils and neutrophils; brittle asthma had more histiocytes-macrophages and lymphocytes.
- Asthma with persistent airflow limitation exhibited significantly increased neutrophil counts.
- Increased expression of M(3)-cholinoreceptor (CHRM3) and histamine H1 receptor (HRH1) genes in brittle asthma.
- Maximal expression of beta(2)-adrenoreceptor (ADRB2) gene observed in asthma with persistent airflow limitation.
Conclusions:
- Significant differences in morphological characteristics exist between severe asthma subtypes.
- Distinct molecular mechanisms of inflammation and bronchoconstriction underlie severe asthma heterogeneity.
- Findings highlight the need for subtype-specific approaches in managing severe asthma.
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