{"title":"Unraveling the role of IL-17A variants in pulmonary tuberculosis: Insights from a case-control study.","authors":"Mahdi Majidpour, Mahboobeh Sabeti Akbar-Abad, Hossein Shahriari, Sajad Barakzaee, Khashayar Zafarmohammadi, Zahra Mohammadghasemipour","doi":"10.1016/j.meegid.2025.105735","DOIUrl":null,"url":null,"abstract":"<p><strong>Objectives: </strong>The present study aimed to investigate the association between certain interleukin-17 A (IL-17 A) polymorphisms, specifically rs2275913 and rs8193036, and the susceptibility to pulmonary tuberculosis (PTB). Considering the function of IL-17 A in regulating immunological responses, especially regarding bacterial infections, we sought to determine if variations in the IL-17 A gene effect on PTB in the examined group.</p><p><strong>Methods: </strong>We performed a case-control study with 100 individuals who were confirmed to have PTB and 100 control subjects. Genotyping for the IL-17 A SNPs rs2275913 and rs8193036 was performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and Tetra-primer Amplification Refractory Mutation System (Tetra-ARMS PCR) methodologies. A statistical analysis encompassing odds ratios (OR) and 95 % confidence intervals (CI) was conducted to assess the association between the polymorphisms and the risk of PTB.</p><p><strong>Results: </strong>Our data indicated a significant connection between the rs2275913 polymorphism and elevated susceptibility to PTB (OR = 1.69, 95 % CI: 1.09-2.61; p = 0.031). Also, a significant association between the rs8193036 polymorphism and increased susceptibility to PTB (OR = 2.18, 95 % CI: 1.46-3.27; p < 0.001).</p><p><strong>Conclusion: </strong>The IL-17 A polymorphisms rs2275913 and rs8193036 strongly correlate with increased susceptibility to PTB, according to this study. This suggests a potential genetic risk factor in the progression of the disease.</p>","PeriodicalId":54986,"journal":{"name":"Infection Genetics and Evolution","volume":" ","pages":"105735"},"PeriodicalIF":2.6000,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Infection Genetics and Evolution","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.meegid.2025.105735","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"INFECTIOUS DISEASES","Score":null,"Total":0}
引用次数: 0
Abstract
Objectives: The present study aimed to investigate the association between certain interleukin-17 A (IL-17 A) polymorphisms, specifically rs2275913 and rs8193036, and the susceptibility to pulmonary tuberculosis (PTB). Considering the function of IL-17 A in regulating immunological responses, especially regarding bacterial infections, we sought to determine if variations in the IL-17 A gene effect on PTB in the examined group.
Methods: We performed a case-control study with 100 individuals who were confirmed to have PTB and 100 control subjects. Genotyping for the IL-17 A SNPs rs2275913 and rs8193036 was performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and Tetra-primer Amplification Refractory Mutation System (Tetra-ARMS PCR) methodologies. A statistical analysis encompassing odds ratios (OR) and 95 % confidence intervals (CI) was conducted to assess the association between the polymorphisms and the risk of PTB.
Results: Our data indicated a significant connection between the rs2275913 polymorphism and elevated susceptibility to PTB (OR = 1.69, 95 % CI: 1.09-2.61; p = 0.031). Also, a significant association between the rs8193036 polymorphism and increased susceptibility to PTB (OR = 2.18, 95 % CI: 1.46-3.27; p < 0.001).
Conclusion: The IL-17 A polymorphisms rs2275913 and rs8193036 strongly correlate with increased susceptibility to PTB, according to this study. This suggests a potential genetic risk factor in the progression of the disease.
期刊介绍：
(aka Journal of Molecular Epidemiology and Evolutionary Genetics of Infectious Diseases -- MEEGID)
Infectious diseases constitute one of the main challenges to medical science in the coming century. The impressive development of molecular megatechnologies and of bioinformatics have greatly increased our knowledge of the evolution, transmission and pathogenicity of infectious diseases. Research has shown that host susceptibility to many infectious diseases has a genetic basis. Furthermore, much is now known on the molecular epidemiology, evolution and virulence of pathogenic agents, as well as their resistance to drugs, vaccines, and antibiotics. Equally, research on the genetics of disease vectors has greatly improved our understanding of their systematics, has increased our capacity to identify target populations for control or intervention, and has provided detailed information on the mechanisms of insecticide resistance.
However, the genetics and evolutionary biology of hosts, pathogens and vectors have tended to develop as three separate fields of research. This artificial compartmentalisation is of concern due to our growing appreciation of the strong co-evolutionary interactions among hosts, pathogens and vectors.
Infection, Genetics and Evolution and its companion congress [MEEGID](http://www.meegidconference.com/) (for Molecular Epidemiology and Evolutionary Genetics of Infectious Diseases) are the main forum acting for the cross-fertilization between evolutionary science and biomedical research on infectious diseases.
Infection, Genetics and Evolution is the only journal that welcomes articles dealing with the genetics and evolutionary biology of hosts, pathogens and vectors, and coevolution processes among them in relation to infection and disease manifestation. All infectious models enter the scope of the journal, including pathogens of humans, animals and plants, either parasites, fungi, bacteria, viruses or prions. The journal welcomes articles dealing with genetics, population genetics, genomics, postgenomics, gene expression, evolutionary biology, population dynamics, mathematical modeling and bioinformatics. We also provide many author benefits, such as free PDFs, a liberal copyright policy, special discounts on Elsevier publications and much more. Please click here for more information on our author services .
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