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About this Research Topic

Manuscript Submission Deadline 30 June 2023
Manuscript Extension Submission Deadline 31 July 2023

Asthma has become a global health issue affecting approximately 4% of the world population. The number of patients suffering from the disorder is expected to reach 400 million worldwide by 2025. The classic allergic airway inflammation is caused by submucosal infiltration of activated T-lymphocytes, ...

Asthma has become a global health issue affecting approximately 4% of the world population. The number of patients suffering from the disorder is expected to reach 400 million worldwide by 2025. The classic allergic airway inflammation is caused by submucosal infiltration of activated T-lymphocytes, eosinophils, neutrophils, epithelial cells, macrophages and mast cells. Thus, initialing the allergic airway inflammation process is a complex web of cells and cell signaling molecules interacting to elicit an inflammatory response. Cellular stress plays a key role in the progression of pathogenesis of allergic asthma such as endoplasmic reticulum stress, mitochondrial stress and oxidative stress. However, the specific mechanism of cellular stress in allergic asthma is complex and currently has not yet been fully clarified.

This Research topic welcomes all article types accepted by Frontiers in Allergy, covering themes including the following:

a.The role and mechanism of mitochondrial stress and metabolic changes in the pathogenesis of asthma.
b.Cellular stress of the bronchial epithelial cells involved in asthma.
c.The relationship and molecular mechanism between cellular stress of immune cells (dendritic cells, macrophages, Th cells, type II lymphocytes, etc.) and the pathogenesis of asthma.
d. Application to asthma treatments

Conflict of interest declaration: Topic Editor Miranda Curtiss is site PI in a clinical trial of dupilumab in Allergic Bronchopulmonary Aspergillosis in asthma patients and has received a grant from the American Lung Association on a mouse model of allergic asthma driven by Aspergillus sensitization.

Keywords: asthma, cellular stress, mitochondrial stress, metabolic, pathogenesis, bronchial epithelial cells, immune cells, treatment, mechanisms


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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