Polymorphisms in Toll-like receptors 1, 2, 5, and 10 are associated with predisposition to Helicobacter pylori infection

Abstract

Objective: Toll-like receptors (TLRs) are significant receptors to the innate immune system which symbolizes a family of pattern recognition receptors. We aimed to investigate associations between rs4833095 polymorphism of TLR1, rs3804099 polymorphism of TLR2, rs5744174 polymorphism of TLR5, and rs10004195 polymorphism of TLR10 in dyspeptic individuals with Helicobacter pylori infection. Methods: Genomic DNA was isolated and genotyping of rs4833095 polymorphism in TLR1, rs3804099 polymorphism in TLR2, rs5744174 polymorphism in TLR5, and rs10004195 polymorphism in TLR10 were investigated in 400 individuals (205 in dyspeptic individuals with H. pylori-positive subjects and 195 dyspeptic individuals with H. pylori-negative subjects) by real-time PCR. Statistical analysis was performed by Pearson’s Chi-square test. Results: According to our study; rs4833095 polymorphism in TLR1 C allele, rs3804099 polymorphism in TLR2 C allele, rs5744174 polymorphism in TLR5 C allele, and rs10004195 polymorphism in TLR10 A allele increased the risk of H. pylori infection [odds ratio (OR), 2.01; 95% confidence interval (CI), 1.39–3.16; OR, 1.78; 95% CI, 1.19–2.6; OR, 1.87; 95% CI, 1.25–2.78; OR, 2.66; 95% CI, 1.72–4.099, respectively]. Conclusion: This is the first study that investigates TLRs in H. pylori infection in Turkey. Our findings may support the hypothesis that polymorphisms in certain TLRs may cause a genetic predisposition to H. pylori-related gastric problems.

No evidence for a causal link between Helicobacter pylori infection and nonalcoholic fatty liver disease: A bidirectional Mendelian randomization study

“…The toll-like receptor 1 (TLR1) gene SNP rs10004195 at 4p14 and the Fc gamma RIIA (FCGR2A) gene SNP rs368433 at 1q23.3 have been identified as the genetic variants for H pylori seroprevalence with the strongest association strength. The A allele of TLR1 has been reported to increase the risk of H. pylori infection ( Tang et al, 2015 ; Kalkanli Tas et al, 2020 ), while FCGR polymorphisms have been implicated in persistent bacterial infections including H. pylori ( Corcoran and Byrne, 2004 ). Furthermore, to examine the strength of the allele scores as instruments, the F statistic for each SNP was approximated from the following equation:…”

The Role of Toll-Like Receptor-2 in Clostridioides difficile Infection: Evidence From a Mouse Model and Clinical Patients

“…The TLR2 rs3804099 polymorphism has been connected to altered host immunity against bacterial infection (36)(37)(38). Of note, in recent years, the TLR2 rs3804099 polymorphism has been thoroughly investigated in association with Helicobacter pylori infection, another important pathogen in gastrointestinal disease (37)(38)(39). In studies in Iran and in Turkey, patients carrying the TLR2 rs3804099 CT genotype more frequently had peptic ulcers and H. pylori infection than healthy individuals (37,39).…”

“…Of note, in recent years, the TLR2 rs3804099 polymorphism has been thoroughly investigated in association with Helicobacter pylori infection, another important pathogen in gastrointestinal disease (37)(38)(39). In studies in Iran and in Turkey, patients carrying the TLR2 rs3804099 CT genotype more frequently had peptic ulcers and H. pylori infection than healthy individuals (37,39). Among individuals infected with H. pylori in Brazil, harboring the TLR2 rs3804099 (19216T/C) polymorphism had a protective effect in gastric carcinogenesis (38).…”

Innate-Immunity Genes in Obesity

“…Microbiome composition in inflammatory bowel disease correlates with rs6871626 near IL12B and intronic rs4246905 of the TNFSF15, a member of the tumor necrosis factor ligand superfamily [235]. Missense variants rs4833095 C of the TLR1 gene and rs5744174 C of the TLR5 gene, synonymous variant rs3804099 C of the TLR2 gene, and 2KB upstream variant rs10004195 A of the TLR10 gene raise the risk of Helicobacter pylori infection [236]. MEVF is an NLR gene coding for a PRR component of the inflammasome complex that can recognize host Rho-GTPase inactivation by various bacterial toxins [237].…”