Interleukin 17 gene in Bronchial Asthma: Review Article | ||||
The Egyptian Journal of Hospital Medicine | ||||
Article 134, Volume 91, Issue 1, April 2023, Page 4632-4638 PDF (649.41 K) | ||||
Document Type: Original Article | ||||
DOI: 10.21608/ejhm.2023.297795 | ||||
View on SCiNiTO | ||||
Authors | ||||
Heba Abdel Hameed Attia Mohamed ; Yousri Mostafa Hussein; Azza Ali Khalil; Abdallah Salem El Deeb | ||||
Abstract | ||||
Background: Asthma patients from all walks of life share a common symptom: persistent airway inflammation. A history of wheezing, chest tightness, shortness of breath, and cough, along with these symptoms, are diagnostic of this condition. Serum levels of interleukin-17 (IL-17) were considerably higher in patients with uncontrolled asthma compared to those with managed asthma and healthy people. Objective: To study and focus on role of IL-17 among bronchial asthma patients. Methods: We scoured medical papers and databases including PubMed, Google Scholar, and Science Direct for information on IL-17 and bronchial asthma. Only the most recent or comprehensive studies conducted between November 2006 and December 2022 were included in the analysis. The authors also assessed the usefulness of references drawn from similar books. Documents written in languages other than English have been neglected because of a lack of funding to translate them. Unpublished articles, oral talks, conference abstracts, and dissertations were all generally agreed upon not to constitute valid scientific investigation. Conclusion: Genetic research, clinical correlations, in vitro investigations, and animal models all point to IL-17 dysregulation as a possible cause of asthma. Asthma is linked to variations in the IL-17 gene in humans. Based on in vitro studies revealing that IL-17 A caused IL-17 receptor alpha expression in human bronchial epithelial cells, the notion was initially proposed that IL-17 A caused airway neutrophilia, a trait of the neutrophilic phenotype. | ||||
Keywords | ||||
Bronchial asthma; IL-17 | ||||
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