Cag pathogenicity island-independent up-regulation of matrix metalloproteinases-9 and -2 secretion and expression in mice by Helicobacter pylori infection
Metadata of CSIR Papers
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| Title |
Cag pathogenicity island-independent up-regulation of matrix metalloproteinases-9 and -2 secretion and expression in mice by Helicobacter pylori infection
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| Creator |
Kundu, P
Mukhopadhyay, AK Patra, R Banerjee, A Berg, DE Swarnakar, S |
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| Subject |
Biochemistry & Molecular Biology
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| Description |
Helicobacter pylori cag pathogenicity island (PAI) is a major determinant of gastric injury via induction of several matrix metalloproteinases (MMPs). In the present study, we examined the influence of the cag PAI on gastric infection and MMP-9 production in mice and in cultured cells. A new mouse colonizing Indian H. pylori strain (AM1) that lacks the cag PAI was used to study the cag PAI importance in inflammation. Groups of C57BL/6 mice were inoculated separately with H. pylori strains AM1 and SS1 (cag(+)), gastric tissues were histologically examined, and bacterial colonization was scored by quantitative culture. Mice infected with either cag(+) or cag(-) H. pylori strains showed gastric inflammation and elevated MMP-3 production. Significant up-regulation of pro-MMP-9 secretion and gene expression in H. pylori infected gastric tissues indicate dispensability of cag PAI for increased pro-MMP-9 secretion and synthesis in mice. In agreement, cell culture studies revealed that both AM1 and SS1 were equipotent in pro-MMP-9 induction in human gastric epithelial cells. Both strains showed moderate increase in MMP-2 activity in vivo and in vitro. In addition, increased secretion of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, and IL-6 induced pro-MMP-9 secretion and synthesis in AM1 or SS1 strain-infected mice suggesting elicitation of pro-inflammatory cytokines by both cag(-) and cag(+) genotype. Moreover, tissue inhibitors of metalloproteinase-1 expression were decreased with increase in pro-MMP-9 induction. These data show that H. pylori may act through different pathways other than cag PAI-mediated for gastric inflammation and contribute to upregulation of MMP-9 via pro-inflammatory cytokines.
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| Publisher |
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INCBETHESDA9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3996 USA
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| Date |
2011-09-20T12:12:04Z
2011-09-20T12:12:04Z 2006 |
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| Type |
Article
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| Identifier |
JOURNAL OF BIOLOGICAL CHEMISTRY
0021-9258 http://hdl.handle.net/123456789/14108 |
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| Language |
English
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