Abstract
Bronchial asthma is primarily caused by sensitization to specific antigens that activate type 2 helper T cells (Th2) through acquired immunity, leading to chronic inflammation due to eosinophilic infiltration. Consequently, inhaled steroids have become an established standard treatment. However, refractory cases that do not respond to this treatment pose a challenge. Recent studies have revealed that neutrophils and type-2 innate lymphoid cells (ILC2) are steroid-resistant. The association between these cells and refractory severe asthma has garnered considerable attention. Therefore, my research focused on investigating the interplay among neuro-endocrine, -immune, and -epithelial cells to understand the pathology of refractory asthma, particularly steroid resistance, and to develop therapeutic medications. So far, I have elucidated the mechanism of the onset of neutrophilic airway inflammation due to stress and discovered the role of interleukin-1β, which could be a therapeutic target. Additionally, I have investigated the activation of ILC2 by pulmonary neuroendocrine cells, the release of calcitonin gene-related peptide (CGRP), and the efficacy of treatments for this condition. In this review, I outline treatment targets and approaches from a novel perspective to address severe refractory asthma focusing on my research findings.
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call