TLR5 dependent gene expression in H. pylori infection
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ABSTRACT:
PROVIDER: PRJNA509419 | ENA |
REPOSITORIES: ENA
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Project description:HEK293 cells overexpressing TLR5 (TLR5+) and parent cell lines were infected with H. pylori to differentiate the gene expression through increased TLR5 signalling.
2019-10-22 | GSE123623 | 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:Toll-like receptor TLR5 recognizes a conserved domain, termed D1, that is present in flagellins of several pathogenic bacteria but not in Helicobacter pylori. Highly virulent H. pylori strains possess a type IV secretion system (T4SS) for delivery of virulence factors into gastric epithelial cells. Here, we show that one of the H. pylori T4SS components, protein CagL, can act as a flagellin-independent TLR5 activator. CagL contains a D1-like motif that mediates adherence to TLR5+ epithelial cells, TLR5 activation, and downstream signaling in vitro. TLR5 expression is associated with H. pylori infection and gastric lesions in human biopsies. Using Tlr5-knockout and wild-type mice, we show that TLR5 is important for efficient control of H. pylori infection. Our results indicate that CagL, by activating TLR5, may modulate immune responses to H. pylori.
| S-EPMC6915727 | biostudies-literature
Project description:Carcinogenic bacteria, Helicobacter pylori, induce DNA double-strand breaks in infected host cells, while ATM-dependent DNA damage responses in host cells suppress genome instabilities caused by DNA breakages, which resulting in the suppression of H. pylori-induced gastric cancers. Although Helicobacter pylori infection is etiologically related to the inflammation-related malignancy, gastric cancers, it role in the molecular pathogenesis of disease remains unclear. In vitro studies have suggested the infection may cause breaks in double-stranded DNA. We used microarray analysis of H. pylori-infected human gastric biopsies to investigate the effect of H. pylori on gene expression genes involved in DNA repair and DNA damage response. Micro-array analysis and immunohistochemistory showed that ATM (ataxia-telangiectasia mutated) was upregulated in H. pylori gastritis but down regulated in the premalignant lesion, intestinal metaplasia. Studies in gastric cancer cell lines showed that H. pylori-infection induced activation of ATM and formation of γ-H2AX. γ-H2AX formation was present following infection with bout cag pathogenicity island (PAI)- positive and negative strains but more robust with cag PAI positive strains consistent with the fact that both cag PAI positive negative strains are associated with gastric cancer but the risk is higher with cag PAI positive strains. Eradication of H. pylori infection is associated with a reduction in cancer risk even in the most high risk populations. These data provide a plausible molecular mechanism for a direct bacterial-host interaction increasing cancer risk. To identify tumor suppressors affected by H. pylori-infection, microarray screening was used to compare the gene expression profiles of gastric mucosa obtained from individuals with H. pylori-gastritis and with intestinal metaplasia with tissue from uninfected controls.
2014-08-18 | E-GEOD-47797 | biostudies-arrayexpress
Project description:The cell surface mucin MUC1 is an important host factor limiting Helicobacter pylori (H. pylori) pathogenesis in both humans and mice by providing a protective barrier and modulating mucosal epithelial and leukocyte responses. We used microarrays to detail the global programme of gene expression in Wild type and MUC1- deficient mice in response to H. pylori infection.
2020-05-30 | GSE151418 | GEO
Project description:Carcinogenic bacteria, Helicobacter pylori, induce DNA double-strand breaks in infected host cells, while ATM-dependent DNA damage responses in host cells suppress genome instabilities caused by DNA breakages, which resulting in the suppression of H. pylori-induced gastric cancers. Although Helicobacter pylori infection is etiologically related to the inflammation-related malignancy, gastric cancers, it role in the molecular pathogenesis of disease remains unclear. In vitro studies have suggested the infection may cause breaks in double-stranded DNA. We used microarray analysis of H. pylori-infected human gastric biopsies to investigate the effect of H. pylori on gene expression genes involved in DNA repair and DNA damage response. Micro-array analysis and immunohistochemistory showed that ATM (ataxia-telangiectasia mutated) was upregulated in H. pylori gastritis but down regulated in the premalignant lesion, intestinal metaplasia. Studies in gastric cancer cell lines showed that H. pylori-infection induced activation of ATM and formation of γ-H2AX. γ-H2AX formation was present following infection with bout cag pathogenicity island (PAI)- positive and negative strains but more robust with cag PAI positive strains consistent with the fact that both cag PAI positive negative strains are associated with gastric cancer but the risk is higher with cag PAI positive strains. Eradication of H. pylori infection is associated with a reduction in cancer risk even in the most high risk populations. These data provide a plausible molecular mechanism for a direct bacterial-host interaction increasing cancer risk.
2014-08-23 | GSE60662 | GEO
Project description:Carcinogenic bacteria, Helicobacter pylori, induce DNA double-strand breaks in infected host cells, while ATM-dependent DNA damage responses in host cells suppress genome instabilities caused by DNA breakages, which resulting in the suppression of H. pylori-induced gastric cancers. Although Helicobacter pylori infection is etiologically related to the inflammation-related malignancy, gastric cancers, it role in the molecular pathogenesis of disease remains unclear. In vitro studies have suggested the infection may cause breaks in double-stranded DNA. We used microarray analysis of H. pylori-infected human gastric biopsies to investigate the effect of H. pylori on gene expression genes involved in DNA repair and DNA damage response. Micro-array analysis and immunohistochemistory showed that ATM (ataxia-telangiectasia mutated) was upregulated in H. pylori gastritis but down regulated in the premalignant lesion, intestinal metaplasia. Studies in gastric cancer cell lines showed that H. pylori-infection induced activation of ATM and formation of γ-H2AX. γ-H2AX formation was present following infection with bout cag pathogenicity island (PAI)- positive and negative strains but more robust with cag PAI positive strains consistent with the fact that both cag PAI positive negative strains are associated with gastric cancer but the risk is higher with cag PAI positive strains. Eradication of H. pylori infection is associated with a reduction in cancer risk even in the most high risk populations. These data provide a plausible molecular mechanism for a direct bacterial-host interaction increasing cancer risk. To identify tumor suppressors affected by H. pylori-infection, microarray screening was used to compare the gene expression profiles of gastric mucosa obtained from individuals with H. pylori-gastritis and with intestinal metaplasia with tissue from uninfected controls.
2014-08-23 | E-GEOD-60662 | biostudies-arrayexpress
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:Activators of innate immunity may have potential to combat a broad range of infectious agents. We report that treatment with bacterial flagellin prevented rotavirus (RV) infection in mice and cured chronically RV-infected mice. Protection was independent of adaptive immunity and interferon (IFN, type I and II) and required flagellin receptors Toll-like receptor 5 (TLR5) and NOD-like receptor C4 (NLRC4). Flagellin-induced activation of TLR5 on dendritic cells elicited production of the cytokine interleukin (IL)-22, which induced a protective gene expression program in intestinal epithelial cells. Flagellin also induced NLRC4-dependent production of IL-18 and immediate elimination of RV-infected cells. Administration of IL-22 and IL-18 to mice fully recapitulated the capacity of flagellin to prevent or eliminate RV infection, and thus holds promise as a broad-spectrum antiviral agent.
2014-11-30 | GSE62479 | GEO
Project description:Increased researches show that complement, the codominant central mediator of humoral immunity, is a critical factor in tumor initiation, development, and chemotherapy resistance. C5a/C5aR1 signaling has been shown to promote tumor progression by recruiting MDSCs in breast malignancies And blockade of C5aR1 resets M1 via gut microbiota-mediated PFKM stabilization in a TLR5-dependent manner. We here report that TLR5 as a key regulator of tumor associated macrophages M1 polarization. Flagellin, the protein subunit of the bacterial flagellum, stimulates the innate immune receptor Toll-like receptor 5 (TLR5) after pattern recognition. Receptor activity was turned by a TLR5-flagellin interaction distal to the site of pattern recognition. Thus, activation of downstream signaling pathway is promoted.
2024-01-20 | GSE252048 | GEO