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厄瓜多尔人群中与免疫反应识别和诱导相关的膜受体基因变异与幽门螺杆菌感染的关联

Association of genetic variants of membrane receptors related to recognition and induction of immune response with Helicobacter pylori infection in Ecuadorian individuals.

作者信息

Cabrera-Andrade A, López-Cortés A, Muñoz M J, Jaramillo-Koupermann G, Rodriguez O, Leone P E, Paz-y-Miño C

机构信息

Biomedical Research Institute, School of Health Science, Universidad de las Américas, Quito, Ecuador.

出版信息

Int J Immunogenet. 2014 Aug;41(4):281-8. doi: 10.1111/iji.12118. Epub 2014 Apr 23.

Abstract

Helicobacter pylori (Hp) has a worldwide distribution showing its higher prevalence of infection in developing countries. Toll-like receptors (TLRs) and C-type lectin receptors (CLRs) are proteins that recognize pathogen-associated molecular patterns (PAMPs) and initiate an innate immune response by promoting growth and differentiation of specialized hematopoietic cells for host defense. Gastric infections led by Hp induce a Th-1 cellular immune response, regulated mainly by the expression of IFN-γ. In this retrospective case-control study, we evaluated the TLR1 1805T/G, TLR2 2029C/T, TLR4 896A/G, CD209 -336A/G and IFNGR1 -56C/T polymorphisms and their relationship with susceptibility to Hp infection. TLR1 1805T/G showed statistical differences when the control (Hp-) and infected (Hp+) groups (P = 0.041*) were compared; the TLR1 1805G allele had a protective effect towards infection (OR = 0.1; 95% CI = 0.01-0.88, P = 0.033*). Similarly, the IFNGR1 -56C/T polymorphism showed statistical differences between Hp+ and Hp- (P = 0.018*), and the IFNGR1 -56TT genotype exhibited significant risk to Hp infection (OR = 2.9, 95% CI = 1.27-6.54, P = 0.018*). In conclusion, the pro-inflammatory TLR1 1805T and IFNGR1 -56T alleles are related with susceptibility to Hp infection in Ecuadorian individuals. The presence of these polymorphisms in individuals with chronic infection increases the risk of cellular damage and diminishes the cellular immune response efficiency towards colonizing agents.

摘要

幽门螺杆菌(Hp)在全球范围内均有分布,在发展中国家的感染率更高。Toll样受体(TLRs)和C型凝集素受体(CLRs)是识别病原体相关分子模式(PAMPs)的蛋白质,通过促进特定造血细胞的生长和分化来启动先天性免疫反应,以进行宿主防御。由Hp引起的胃部感染会诱导Th-1细胞免疫反应,主要受IFN-γ表达的调节。在这项回顾性病例对照研究中,我们评估了TLR1 1805T/G、TLR2 2029C/T、TLR4 896A/G、CD209 -336A/G和IFNGR1 -56C/T多态性及其与Hp感染易感性的关系。比较对照组(Hp-)和感染组(Hp+)时,TLR1 1805T/G显示出统计学差异(P = 0.041*);TLR1 1805G等位基因对感染具有保护作用(OR = 0.1;95% CI = 0.01-0.88,P = 0.033*)。同样,IFNGR1 -56C/T多态性在Hp+和Hp-之间显示出统计学差异(P = 0.018*),并且IFNGR1 -56TT基因型对Hp感染表现出显著风险(OR = 2.9,95% CI = 1.27-6.54,P = 0.018*)。总之,促炎性TLR1 1805T和IFNGR1 -56T等位基因与厄瓜多尔个体对Hp感染的易感性有关。慢性感染个体中这些多态性的存在会增加细胞损伤的风险,并降低对定植病原体的细胞免疫反应效率。

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