TLR5 dependent gene expression in H. pylori infection
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE123623 | GEO | 2019/10/22
REPOSITORIES: GEO
Dataset's files
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| GSE123623_RAW.tar | Raw | |||
| GSE123623_SP_K1701_A4835_intensity_norm_rev.xls.gz | Xls | |||
| filelist.txt | Txt |
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Project description:TLR5 dependent gene expression in H. pylori infection
| PRJNA509419 | ENA
Project description:Our previous study has found the VacA virulence of Helicobacter pylori could induce the apoptosis of gastric epithelial cells and TRAF1 plays a crucial role in this process. In order to further investigate the detailed mechanism of TRAF1-related apoptosis, we constructed a TRAF1 knockdown model in MKN74 cells and TRAF1 overexpressing model in HGC27 cells.
2025-03-05 | GSE290844 | GEO
Project description:Helicobacter pylori (H. pylori) is a human pathogen that infects almost half of the world’s population. Infection with H. pylori is frequently associated with chronic gastritis and can even lead to gastric and duodenal ulcers and gastric cancer. Although the persistent colonization of H. pylori and the development of H. pylori-associated gastritis remain poorly understood, it is believed that, in gastric mucosa, the modulated gastric epithelial cells (GECs) by H. pylori are key contributors. We used microarrays to detail the global programme of gene expression in Helicobacter pylori infected-gastric epithelial cell line AGS cells and identified up-regulated genes induced by Helicobacter pylori infection.
2024-04-18 | GSE264263 | GEO
Project description:Helicobacter pylori is a highly successful and important human pathogen that causes chronic gastritis, peptic ulcer diseases and gastric cancer. Innate immunity plays an important role of the primary defense against pathogens and epidemiological studies have suggested a role of toll-like receptor 1 (TLR1) in the risk of H. pylori acquisition. We performed microarray analysis of gastric mucosal biopsy specimens from H. pylori-positive and uninfected subjects; infection was associated with an ~15-fold up-regulation of TLR10 (p <0.001). Quantitative RT-PCR confirmed TLR10 mRNA levels were increased 3-fold in H. pylori-infection (p <0.001) and immunohistochemistory using anti-TLR10 polyclonal antibodies showed increased TLR10 expression in gastric epithelial cells of infected individuals. In vitro experiments where H. pylori was co-cultured with NCI-N87 gastric cells showed significant H. pylori-specific up-regulation of TLR10 mRNA levels and a correlation with TLR2 mRNA levels (R = 0.87, P <0.001). We compared combinations of TLRs for their ability to mediate NF-_B activation. NF-_B activation was increased following exposure to heat killed H. pylori or H. pylori-LPS only with the TLR2/TLR10 heterodimer. These findings suggest TLR10 is a functional receptor involved in the innate immune response to H. pylori infection and that TLR2/TLR10 heterodimer possibly functions in the recognition of H. pylori-LPS.
2015-06-01 | GSE60427 | GEO
Project description:The HT29 derivative cell line HT29-MTX-E12 (E12) produces an adherent mucus layer predominantly of the gastric MUC5AC mucin when grown on transwells. This mucus layer supports Helicobacter pylori survival in culture. E12 cells were infected with H. pylori and the transcriptome of infected and uninfected E12 were compared. Also included for comparison was the HT29 parent cell line grown on transwells. The study focused on glycosylation related genes as these regulate the structures that have a major role to play in pathogen-host cell interaction.
2017-09-21 | GSE74492 | GEO
Project description: Not available
| S-EPMC6915727 | biostudies-literature
Project description:Toll-like receptor 5 (TLR5) plays a critical role beyond its traditional function in innate immunity, significantly impacting metabolic regulation and liver health. Previously, we reported that TLR5 activation extends healthspan and lifespan in aging mice. This study demonstrates that TLR5 deficiency leads to pronounced metabolic abnormalities with age, primarily affecting liver metabolic functions rather than intestinal inflammation. Comprehensive RNA sequencing analysis revealed that TLR5 deficiency induces gene expression changes in liver tissue similar to those caused by the methionine-choline deficient (MCD) diet, particularly affecting lipid metabolism and circadian rhythm-related genes. TLR5 KO mice displayed an increased propensity for liver fibrosis and lipid accumulation under the MCD diet, exacerbating liver pathology. Both hepatocytes and hepatic stellate cells in TLR5 KO mice were functionally impacted, leading to metabolic dysfunction and fibrosis. These findings suggest that TLR5 could be a significant target for addressing metabolic diseases that arise and worsen with aging. Furthermore, understanding the mechanisms by which TLR5 activation extends healthspan could provide valuable insights into therapeutic strategies for enhancing longevity and managing age-related metabolic disorders.
2025-06-18 | GSE272622 | GEO
Project description:<p>BACKGROUND: The gut microbiome and the host immune system interact synergistically to maintain intestinal health and defend against infections. Toll-like receptor 5 (TLR5), known for recognizing bacterial flagellin, plays a pivotal role in this regulatory network. Despite significant advances in understanding the gut microbiome and TLR5, the precise role of TLR5 in gut health and infection resistance remains unclear. This study aimed to elucidate the role of TLR5 in regulating gut microbiota and metabolites and their impact on resistance to Salmonella infection using a TLR5 intestinal-specific overexpression mouse model. </p><p>METHODS: Fecal microbiota and metabolite transplantation experiments were conducted using feces from TLR5-overexpressing mice (TLR5+/+ group) and wild-type mice (WT group) into C57 mice, creating four experimental groups: Flora-TLR5-C57, Metabolite-TLR5-C57, Flora-WT-C57 and Metabolite-WT-C57. Mice were infected with Salmonella, and various parameters including survival time, fecal Salmonella load, and alterations in gut microbiota and metabolites were assessed. </p><p>RESULTS: Despite notable shifts in gut microbiota composition and metabolite profiles induced by TLR5 overexpression, no significant differences in fecal Salmonella load or survival time were observed across the experimental groups. TLR5-overexpressing mice exhibited an enrichment of beneficial bacterial taxa and significant changes in metabolites; however, these alterations did not correlate with enhanced resistance to Salmonella infection. </p><p>CONCLUSION: Our findings suggest that while TLR5 overexpression significantly modifies gut microbiota and metabolite profiles, these changes do not directly enhance resistance to Salmonella infection. The immune response to Salmonella is multifaceted and involves various components beyond the gut microbiota and metabolites. Further research is required to elucidate the detailed molecular pathways through which TLR5 influences infection outcomes and to explore potential combined therapeutic strategies for enhancing host defenses against enteric pathogens.</p>
2024-07-25 | MTBLS10592 | MetaboLights
Project description:Gram negative bacteria release outer membrane vesicles (OMVs) as part of their natural growth. These OMVs take part in a biological functions including bacterial communication, exchange of genetic material and bacterial pathogenesis. However, the relationship between bacterial growth stage and OMV protein composition has not been explored before nor how their proteome is different to their parent bacterium. In this study, we examined the proteome of Helicobacter pylori and its OMVs from early log, late log or stationary phase of growth and found that globally, the protein content of OMVs over time is vastly different to one another as well as to their parent bacterium. OMVs purified from early log phase of growth contained the greatest number of unique proteins and a significant upregulation of virulence and pathogenic proteins. However, when compared back to their parent bacterium, OMVs from later stages of growth contained more unique proteins than those from earlier stages of growth. We show for the first time the regulation of OMV protein composition by H. pylori that is dependent on bacterial growth stage. Our results have expanded our understanding of the fundamental production of OMVs and the selective packaging of cargo in OMVs that result in specific functions.
2021-03-23 | PXD024918 | Pride
Project description:Based on preliminary data demonstrating that macrophages are critical regulators of Helicobacter pylori colonization and gastric pathology in mice, we sought to investigate how macrophages may serve as bacterial reservoirs of intracellular H. pylori.
2017-02-10 | GSE67270 | GEO