Leptin receptor polymorphism in patients with asthma and its correlation with the disease progression

• Main Authors: Yu-Ming Qiu, Jian-Xiong Li, Cai-Xiang Chen
• Format: Article
• Language: English
• Published: Editorial Board of Journal of Hainan Medical University 2018-10-01
• Series: Journal of Hainan Medical University
• Subjects: Bronchial asthma; Lptin receptor; Gene polymorphism; Inflammatory response; Immune response
• Online Access: http://www.hnykdxxb.com/PDF/201810/06.pdf

Objective: To study the leptin receptor Gln223Arg locus polymorphism in patients with asthma and its correlation with the disease progression. Methods: The patients who were diagnosed with bronchial asthma in our hospital between July 2014 and April 2017 were selected as the asthma group for the study, and the healthy volunteers who received physical examination in our hospital during the same period were selected as the control group. The leptin receptor gene Gln223Arg locus polymorphism was determined, and the contents of inflammatory mediators and airway remodeling indexes in serum as well as the contents of immune cells in peripheral blood were determined. Results: Eotaxin, Galectin-3, YKL- 40, SAA, IL-33, ADAM33, NE and MMP9 contents in serum as well as Th17, Th9 and Tfh contents in peripheral blood of asthma group of patients with AA+AG genotype and GG genotype were significantly higher than those of control group whereas TIMP1 and TIMP2 contents in serum as well as Treg contents in peripheral blood were significantly lower than those of control group; Eotaxin, Galectin-3, YKL-40, SAA, IL-33, ADAM33, NE and MMP9 contents in serum as well as Th17, Th9 and Tfh contents in peripheral blood of asthma group of patients with AA+AG genotype were significantly higher than those of patients with GG genotype whereas TIMP1 and TIMP2 contents in serum as well as Treg content in peripheral blood were significantly lower than those of patients with GG genotype. Conclusion: The substitution from leptin receptor Gln223Arg locus polymorphism A→G replacement in patients with asthma can aggravate the inflammatory response and immune response disorder as well as airway remodeling.