Role of STAT3 Transcription Factor in Pathogenesis of Bronchial Asthma

Role of STAT3 Transcription Factor in Pathogenesis of Bronchial Asthma

Bronchial asthma is a heterogeneous chronic inflammatory disease of airways. The studies of molecular and cellular mechanisms of bronchial asthma have established that a wide range of immune (T and B cells, eosinophils, neutrophils, macrophages, etc.) and structural (epithelial and endothelial) cell...

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Bibliographic Details
Published in:Biochemistry (Moscow) Vol. 86; no. 11; pp. 1489 - 1501
Main Authors: Nikolskii, Aleksandr A., Shilovskiy, Igor P., Barvinskaia, Ekaterina D., Korneev, Artem V., Sundukova, Maria S., Khaitov, Musa R.
Format: Journal Article
Language:English
Published: Moscow Pleiades Publishing 01-11-2021
Springer
Springer Nature B.V
Subjects:
Allergens
Animals
Asthma
Asthma - immunology
Asthma - pathology
B cells
Biochemistry
Biomedical and Life Sciences
Biomedicine
Bioorganic Chemistry
Cell activation
Chemokines
Cytokines
DNA binding proteins
Endothelial cells
Eosinophils
External stimuli
Genetic aspects
Helper cells
Humans
Hyperreactivity
Hypersensitivity
Inflammation
Inflammatory diseases
Leukocytes (eosinophilic)
Leukocytes (neutrophilic)
Leukocytes - immunology
Leukocytes - pathology
Life Sciences
Lung - immunology
Lung - pathology
Lungs
Lymphocytes B
Lymphocytes T
Macrophages
Medical research
Medicine, Experimental
Microbiology
Neutrophils
Pathogenesis
Pollutants
Respiratory tract
Review
Signs and symptoms
Stat3 protein
STAT3 Transcription Factor - immunology
Therapeutic targets
Transcription factors
signaling pathway
bronchial asthma
JAK
T-helpers
STAT3
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Summary:Bronchial asthma is a heterogeneous chronic inflammatory disease of airways. The studies of molecular and cellular mechanisms of bronchial asthma have established that a wide range of immune (T and B cells, eosinophils, neutrophils, macrophages, etc.) and structural (epithelial and endothelial) cells are involved in its pathogenesis. These cells are activated in response to external stimuli (bacteria, viruses, allergens, and other pollutants) and produce pro-inflammatory factors (cytokines, chemokines, metalloproteinases, etc.), which ultimately leads to the initiation of pathological processes in the lungs. Genes encoding transcription factors of the STAT family (signal transducer and activator of transcription), that includes seven representatives, are involved in the cell activation. Recent studies have shown that the transcription factor STAT3 plays an important role in the activation of the abovementioned cells, thus contributing to the development of asthma. In animal studies, selective inhibition of STAT3 significantly reduces the severity of lung inflammation, which indicates its potential as a therapeutic target. In this review, we describe the mechanisms of STAT3 activation and its role in polarization of Th2/Th17 cells and M2 macrophages, as well as in the dysfunction of endothelial cells, which ultimately leads to development of bronchial asthma symptoms, such as infiltration of neutrophils and eosinophils into the lungs, bronchial hyperreactivity, and the respiratory tract remodeling.
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ISSN:0006-2979
1608-3040
DOI:10.1134/S0006297921110122