Objectives: The purpose of this study was to evaluate the effects of interleukin-13 (IL-13) polymorphisms on the risk of asthma using a meta-analysis.
Design And Methods: Fifteen publications were identified by searching Pubmed, Embase, ISI, OVID, and EBSCO databases. Odds ratios with corresponding 95% confidence intervals were computed to estimate the association between IL-13 polymorphisms and risk of asthma.
Results: The polymorphisms of R130Q (rs20541) and -1112C/T (rs1800925) in IL-13 gene were associated with significantly increased risks of asthma in overall analyses. Subgroup analyses showed that the elevated risks occurred in adult-onset asthma, Caucasians, and high quality studies.
Conclusions: This meta-analysis provides evidence that the R130Q and -1112C/T polymorphisms in IL-13 are risk factors for asthma.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.clinbiochem.2011.12.012 | DOI Listing |
Mol Biol Res Commun
January 2025
Department of Pathology, College of Medicine, Qassim University, Saudi Arabia.
Cytokine
December 2024
First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China; National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin, China. Electronic address:
Background: Based on previous research, it is well-established that myasthenia gravis (MG) is linked to chronic inflammation. However, the exact nature of the relationship between inflammatory factors and the development of MG remains unclear. Consequently, the objective of this study is to explore whether alterations in the levels of inflammatory factors, as influenced by genetic factors, are associated with the occurrence of MG.
View Article and Find Full Text PDFRespir Med
December 2024
Department of Pulmonary and Critical Care Medicine, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou 570311, Hainan, China. Electronic address:
Background: Chronic obstructive pulmonary disease (COPD) is characterized by persistent respiratory symptoms and airflow limitation. Interleukin-13 (IL13), associated with T-helper type 2 cells, plays a crucial role in COPD pathophysiology. This study aimed to investigate the relationship of single nucleotide polymorphisms (SNPs) in IL13 to COPD risk.
View Article and Find Full Text PDFCytokine
January 2025
Department of Dermatology, Hunan Engineering Research Center of Skin Health and Disease, Hunan Key Laboratory of Skin Cancer and Psoriasis, Xiangya Hospital, Central South University, Changsha, Hunan, China; National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China. Electronic address:
Background: Previous observational studies have reported that systemic cytokines are associated with the risk of inflammatory skin diseases, but their conclusions remain controversial.
Method: We conducted a two-sample Mendelian randomization analysis to assess the relationship between systemic cytokines and six inflammatory skin disorders (including alopecia areata (AA), acne, atopic dermatitis (AD), hidradenitis suppurativa (HS), psoriasis (PS) and vitiligo), based on datasets from EArly Genetics and Lifecourse Epidemiology (EAGLE) eczema consortium, acne GWAS conducted by Maris Teder Laving et al., IEU Open GWAS, and FinnGen database.
Gene
February 2025
Departamento de Biorregulação, Instituto de Ciências da Saúde, Universidade Federal da Bahia, Bahia, Brazil. Electronic address:
Asthma is a complex disease characterized by reversible and intermittent airway obstruction that has shown a high prevalence and unacceptable mortality in adults. In recent years, several genome-wide association studies (GWAS) have identified variants linked to asthma susceptibility. The DAD1 gene is known for regulating programmed cell death, and OXA1L is described for its involvement in mitochondrial biogenesis and oxidative phosphorylation.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!