Molecular Alterations in Fibroblasts Exposed to <i>Helicobacter pylori</i> Broth Culture Filtrate: A Potential Trigger of Autoimmunity?

Scotti, Claudia; Mignosi, Paola; Filipazzi, Paola; Lazzé, Maria Claudia; Savio, Monica; Cappelletti, Donata; Pasquetto, Maria Valentina; Solcia, Enrico; Vannini, Vanio; Sommi, Patrizia

doi:10.1111/j.1523-5378.2009.00733.x

Cited by 5 publications

(8 citation statements)

References 5 publications

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“…Thus, examining GMF is necessary to understand the T cell responses in the gastric mucosa. Moreover, contact between H. pylori and stromal cells in mucosa is plausible because the mucosal barrier is disrupted during infection, gastritis, and ulceration leading to the transit of bacterial material and entire bacteria from lumen to the sub-epithelial mucosal layer [41], [42]. Thus, our study supports the hypothesis that GMFs contribute to the Th17 increase observed during H. pylori -associated chronic inflammation and gastric cancer.…”

Section: Discussionsupporting

confidence: 83%

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Stromal Cells Induce Th17 during Helicobacter pylori Infection and in the Gastric Tumor Microenvironment

et al. 2013

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Gastric cancer is associated with chronic inflammation and Helicobacter pylori infection. Th17 cells are CD4+ T cells associated with infections and inflammation; but their role and mechanism of induction during carcinogenesis is not understood. Gastric myofibroblasts/fibroblasts (GMF) are abundant class II MHC expressing cells that act as novel antigen presenting cells. Here we have demonstrated the accumulation of Th17 in H. pylori-infected human tissues and in the gastric tumor microenvironment. GMF isolated from human gastric cancer and H. pylori infected tissues co-cultured with CD4+ T cells induced substantially higher levels of Th17 than GMF from normal tissues in an IL-6, TGF-β, and IL-21 dependent manner. Th17 required interaction with class II MHC on GMF for activation and proliferation. These studies suggest that Th17 are induced during both H. pylori infection and gastric cancer in the inflammatory milieu of gastric stroma and may be an important link between inflammation and carcinogenesis.

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Section: Discussionsupporting

confidence: 83%

“…However, we were able to culture similar amounts of α-SMA cells from normal and tumor tissues. Since it has been shown that H. pylori disrupts barrier function, infection may affect GMF as well as epithelium [21]. Hence, we found the class II MHC molecule, HLA-DR to be upregulated by H. pylori on these cells ( Figure 2B ).…”

Section: Resultsmentioning

confidence: 59%

Stromal Cells Induce Th17 during Helicobacter pylori Infection and in the Gastric Tumor Microenvironment

et al. 2013

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“…Such molecular alterations have been linked to the induction of autoimmunity (Krzysiek-Maczka et al, 2013, Scotti et al, 2010.…”

Section: Accepted Manuscriptmentioning

confidence: 98%

“…Amongst the microbial agents, Helicobacter pylori (Hp) has been considered a possible infectious trigger of the disease (Smyk et al, 2014). At the antigen level, several Hp antigens have been considered important for the loss of immunological tolerance to myelin antigens, particularly heat shock proteins (hsp) (Chiba et al, 2006, Panchapakesan et al, 1992, Salvetti et al, 1992, Scotti et al, 2010, Tishler and Shoenfeld, 1996. Several approaches have been used to assess whether hsps are implicated in the pathogenesis of MS, including studies on immune responses to hsp in MS and the extent of cross-reactivity between hsp and CNS myelin, as well as the expression of hsps in the brain of patients with MS (Salvetti et al, 1992, Tishler and Shoenfeld, 1996, Horvath et al, 2001, Gruber et al, 1996, Chiba et al, 2006.…”

Section: Introductionmentioning

confidence: 99%

Anti-hsp60 antibody responses based on Helicobacter pylori in patients with multiple sclerosis: (ir)Relevance to disease pathogenesis

Efthymiou

Dardiotis

Liaskos

et al. 2016

Journal of Neuroimmunology

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“…CAFs may enhance invasion of the cancer cells through expression of TGF β, potent EMT inducer, and HGF, which has been shown to promote breast tumorigenesis 39, 40. Since fibroblasts may alter the mRNA expression of structural and cell cycle‐associated genes in the presence of H. pylori ,9, 41 we have attempted to determine whether H. pylori can interact with fibroblasts by changing them not only into myofibroblasts, but also into CAFs, further being capable of inducing EMT program in normal RGM‐1 epithelial cell line.…”

Section: Introductionmentioning

confidence: 99%

Role of Helicobacter pylori infection in cancer‐associated fibroblast‐induced epithelial‐mesenchymal transition in vitro

et al. 2018

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BackgroundMajor human gastrointestinal pathogen Helicobacter pylori (H. pylori) colonizes the gastric mucosa causing inflammation and severe complications including cancer, but the involvement of fibroblasts in the pathogenesis of these disorders in H. pylori‐infected stomach has been little studied. Normal stroma contains few fibroblasts, especially myofibroblasts. Their number rapidly increases in the reactive stroma surrounding inflammatory region and neoplastic tissue; however, the interaction between H. pylori and fibroblasts remains unknown. We determined the effect of coincubation of normal rat gastric fibroblasts with alive H. pylori (cagA+vacA+) and H. pylori (cagA−vacA−) strains on the differentiation of these fibroblasts into cells possessing characteristics of cancer‐associated fibroblasts (CAFs) able to induce epithelial‐mesenchymal transition (EMT) of normal rat gastric epithelial cells (RGM‐1).Materials and MethodsThe panel of CAFs markers mRNA was analyzed in H. pylori (cagA+vacA+)‐infected fibroblasts by RT‐PCR. After insert coculture of differentiated fibroblasts with RGM‐1 cells from 24 up to 48, 72, and 96 hours, the mRNA expression for EMT‐associated genes was analyzed by RT‐PCR.ResultsThe mRNA expression for CAFs markers was significantly increased after 72 hours of infection with H. pylori (cagA+vacA+) but not H. pylori (cagA−vacA−) strain. Following coculture with CAFs, RGM‐1 cells showed significant decrease in E‐cadherin mRNA, and the parallel increase in the expression of Twist and Snail transcription factors mRNA was observed along with the overexpression of mRNAs for TGFβR, HGFR, FGFR, N‐cadherin, vimentin, α‐SMA, VEGF, and integrin‐β1.Conclusion Helicobacter pylori (cagA+vacA+) strain induces differentiation of normal fibroblasts into CAFs, likely to initiate the EMT process in RGM‐1 epithelial cell line.

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Molecular Alterations in Fibroblasts Exposed to Helicobacter pylori Broth Culture Filtrate: A Potential Trigger of Autoimmunity?

Cited by 5 publications

References 5 publications

Stromal Cells Induce Th17 during Helicobacter pylori Infection and in the Gastric Tumor Microenvironment

Stromal Cells Induce Th17 during Helicobacter pylori Infection and in the Gastric Tumor Microenvironment

Anti-hsp60 antibody responses based on Helicobacter pylori in patients with multiple sclerosis: (ir)Relevance to disease pathogenesis

Role of Helicobacter pylori infection in cancer‐associated fibroblast‐induced epithelial‐mesenchymal transition in vitro

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