Background: Several recent studies have provided evidence that polymorphisms in the interleukin-1 (IL1) gene are implicated in tuberculosis (TB). However, results of different studies are inconsistent. The aim of this study was to perform a meta-analysis investigating the association of the IL1B (-511 and +3954) and IL1RN VNTR polymorphisms with TB risk.
Methods: A systematic review of the English literature was conducted by searching Pubmed, Scopus, and ISI Web of Knowledge databases for relevant studies. Pooled odds ratios (OR) with 95 % confidence intervals (CI) were calculated using fixed effects models. Between-study heterogeneity and publication bias were also evaluated.
Results: Nine case-control studies including 3327 participants were reviewed and analyzed. Our results did not indicate any association of the IL1B (-511 and +3954) and IL1RN VNTR polymorphisms with TB risk in the overall populations. The pooled OR of the IL1B -511 polymorphism was 1.09 (95 % CI 0.87-1.36) for the dominant model, 1.11 (0.89-1.38) for the recessive model, 1.15 (0.87-1.50) for the homozygote model, and 1.07 (0.94-1.23) for the allelic comparison model. ORs for the IL1B +3954 and IL1RN VNTR polymorphisms were similar. In subgroup analysis stratified by ethnicity, the results revealed no association between these polymorphisms and TB risk in black people, Asians, and Caucasians, respectively. We did not identify significant between-study heterogeneity across all studies, and there was no evidence of publication bias.
Conclusions: Our results indicate there is a lack of association between the IL1B (-511 and +3954), IL1RN VNTR polymorphisms and TB risk.
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http://dx.doi.org/10.1007/s00408-015-9796-5 | DOI Listing |
Minerva Pediatr (Torino)
November 2024
Network of Immunity in Infection, Malignancies, and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Tehran, Iran -
Introduction: Juvenile idiopathic arthritis (JIA) is one of the most common chronic diseases of childhood and presents with various clinical phenotypes. A multifactorial and complex interaction of genetic and environmental factors are responsible for JIA, of which the proinflammatory cytokine genes are of particular research interest. This meta-analysis investigates the association between IL-1A and IL-1B gene polymorphisms and susceptibility to JIA.
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Diretoria de Ensino e Pesquisa, Fundação Hospitalar de Hematologia e Hemoterapia do Amazonas (HEMOAM), Manaus, Brazil.
The relationship between the (rs16944) polymorphism and the risk of developing hematologic malignancies remains controversial. Thus, we performed a meta-analysis to evaluate the association between polymorphism and the risk of developing hematologic malignancies. A comprehensive search was conducted to identify all eligible studies on polymorphism and hematologic malignancies.
View Article and Find Full Text PDFJ Taibah Univ Med Sci
April 2024
Department of Oral Medicine & Radiology, King George's Medical University, Lucknow, India.
Int J Mol Sci
January 2024
Egas Moniz Center for Interdisciplinary Research (CiiEM), Egas Moniz School of Health & Science, Campus Universitário, Quinta da Granja, 2829-511 Almada, Portugal.
The aim of this study was to evaluate the possible relationships between polymorphisms in the interleukin-1 () , , and genes and concentrations of the inflammatory mediators IL-1β, tumor necrosis factor-alpha (TNF-α), and prostaglandin E2 (PGE2) in peri-implant crevicular fluid (PICF). A cross-sectional analytical study was conducted on 51 patients with dental implants. Samples from the buccal mucosa were obtained, and genetic analysis was performed using the real-time polymerase chain reaction (PCR) technique for and and PCR and restriction fragment length polymorphism analysis for .
View Article and Find Full Text PDFInt J Mol Sci
September 2023
Department of Periodontology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.
Chronic periodontitis is a bacterial infection associated with dentally adherent biofilm (plaque) accumulation and age-related comorbidities. The disease begins as an inflammatory exudate from gingival margins, gingival crevicular fluid (GCF) in response to biofilm lysine. After a week of experimental gingivitis (no oral hygiene), biofilm lysine concentration was linearly related to biofilm accumulation (plaque index) but to GCF as an arch-shaped double curve which separated 9 strong from 6 weak GCF responders (hosts).
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