Aim: To determine if there are significant associations between polymorphisms of the IL-1, IL-6, and IL-10 genes and susceptibility to recurrent aphthous stomatitis (RAS).
Methods: The PubMed, Embase, and Web of Science databases were searched for all eligible studies using both medical subheadings and free terms through December 2016. A total of 226 citations were retrieved. Odds ratios were used to quantitatively evaluate the associations of IL-1, IL-6, and IL-10 gene polymorphisms with RAS risk. A meta-analysis was performed, and heterogeneity, sensitivity, and subgroup analyses were carried out to clarify and validate the pooled results.
Results: A total of 11 studies were identified that met the inclusion criteria and were included in the meta-analysis. This current systematic review indicated that the IL-1b+3954 C/T polymorphism was significantly associated with an elevated risk of RAS onset for all inheritance models, except for the dominant model. For the IL-10-592 C/A polymorphism, protective associations with RAS were found using both the additive and recessive models, while it increased the risk of RAS in the codominant model. In Asian populations, the IL-10-1082 G/A polymorphism was associated with a protective effect for RAS using the allelic, additive, and recessive models. The IL-6-174 G/C polymorphism was not statistically associated with RAS risk.
Conclusion: The IL-1b+3954 C/T polymorphism significantly increases RAS risk. In addition, the IL-10-1082 G/A polymorphism provided protective effects for RAS in the Asian population.
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http://dx.doi.org/10.1089/gtmb.2017.0072 | DOI Listing |
Front Immunol
January 2025
Division for Biochemistry of Joint and Connective Tissue Diseases, Department of Orthopedics, Ulm University Medical Center, Ulm, Germany.
Background: The complement system is locally activated after joint injuries and leads to the deposition of the terminal complement complex (TCC). Sublytic TCC deposition is associated with phenotypical alterations of human articular chondrocytes (hAC) and enhanced release of inflammatory cytokines. Chronic inflammation is a known driver of chondrosenescence in osteoarthritis (OA).
View Article and Find Full Text PDFJ Neuroinflammation
January 2025
Department of Ophthalmology, Wilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Background: The retinal degenerative diseases retinitis pigmentosa (RP) and atrophic age- related macular degeneration (AMD) are characterized by vision loss from photoreceptor (PR) degeneration. Unfortunately, current treatments for these diseases are limited at best. Genetic and other preclinical evidence suggest a relationship between retinal degeneration and inflammation.
View Article and Find Full Text PDFWiad Lek
January 2025
EXPERT-ANALYTICAL MEDICAL CENTER FOR MOLECULAR GENETICS, SHUPYK NATIONAL HEALTHCARE UNIVERSITY OF UKRAINE, KYIV, UKRAINE.
Objective: Aim: To determine the influence of maternal and neonatal variants of the eNOS (G894T, rs1799983) and IL1B (C3953T, rs1143634) genes and their intergenic interactions on the development of HIE in newborns.
Patients And Methods: Materials and Methods: The study included a cohort of 105 newborns and their 99 mothers. Determination of variants of the genes eNOS (G894T, rs1799983) and IL1B (C3953T, rs1143634) was carried out for the patients of study groups.
Backgrounds: Abuse of feed supplement can cause oxidative stress and inflammatory responses in Gallus gallus. Synbiotics are composed of prebiotics and probiotics and it possess huge application potentials in the treatment of animal diseases.
Methods: This study examined the effect of d-tagatose on the probiotic properties of L.
Mol Cancer Res
January 2025
Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
Malignant neoplasms arise within a region of chronic inflammation caused by tissue injuries. Inflammation is a key factor involved in all aspects of tumorigenesis including initiation, proliferation, invasion, angiogenesis, and metastasis. Interleukin-1 (IL-1) plays critical functions in tumor development with influencing the tumor microenvironment and promoting cancer progression.
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