Abstract
The aim of this study was to define the relationship between several environmental, laboratory, and genetic factors, i.e., TLR2 and NLRP3 polymorphisms, and Helicobacter pylori (H. pylori) infection in children, by comparing three different groups of pediatric subjects: H. pylori-induced gastritis, non-H. pylori gastritis, and healthy controls. Our final study sample included 269 children, which were divided into three groups according to the histopathological exam: group 1 with 51 children with H. pylori-induced gastritis, group 2 with 103 children with H. pylori-negative gastritis, and group 3 (control group) with 115 children without any histopathological changes. All children underwent a thorough anamnesis, clinical exam, laboratory tests, and upper digestive endoscopy with gastric biopsy for rapid urease test, histopathological exam, and genetic analysis of TLR2 rs3804099, TLR2 rs3804100, and NLRP3 rs10754558 gene polymorphisms. We noticed a significant association between living conditions and the type of gastritis (p < 0.0001). Both rapid urease and serological tests were significantly associated with the presence of H. pylori (p < 0.0001). The CT variant genotype of TLR2 rs380499 was significantly associated with neutrophil count (p = 0.0325). We noticed a significant association between the CC variant genotype of NLRP3 rs10754558 and leucocytes, neutrophils, eosinophils, as well as ALT (p = 0.0185, p = 0.0379, p = 0.0483, p = 0.0356). Based on these findings, we state that poor living conditions and rural areas represent risk factors for H. pylori infection. The rapid urease test is a reliable diagnostic tool for this infection. CT and TT carriers of TLR2 rs3804099, as well as CC carriers of NLRP3 rs10754558, might display a more severe degree of systemic inflammation.
Highlights
Chronic inflammation is the hallmark of carcinogenesis, playing a crucial role in the development of a wide diversity of solid tumors
We noticed a significant association between living conditions and the type of gastritis (p < 0.0001), indicating that poor living conditions predominated in the group with H. pylori-induced gastritis (35.29%), followed by the group with other types of gastritis (13.59%) versus only 6.96% in the control group
We found no significant differences between the three groups in terms of TLR2 rs3804099, TLR2 rs3804100, and
Summary
Chronic inflammation is the hallmark of carcinogenesis, playing a crucial role in the development of a wide diversity of solid tumors. It is well-documented that this infection might lead to chronic gastritis, peptic ulcers, gastric cancer, and mucosa-associated lymphoid tissue lymphomas [1,2]. It was previously demonstrated that H. pylori-associated inflammation is closely related to the host’s innate immune system since it is capable of triggering these responses via particular pathogenicity features such as cag-pathogenicity island (cagPAI). The combination of PAMPs, toll-like receptors (TLRs), and nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) results in the activation of immune cells receptors and subsequent promotion of both secretion and expression of several proinflammatory cytokines. H. pylori has the ability to upregulate IL-1β and IL-18 in human immune cells and gastric tissue of animal models, proving its impact on the activation of inflammasomes [5,6,7]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
