Linked Life Data

17442980

Source:http://linkedlifedata.com/resource/pubmed/id/17442980

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pubmed-article:17442980pubmed:abstractTextHelicobacter pylori (Hp) infection is associated with gastric inflammation and ulceration. The pathways of tissue damage in Hp-infected subjects are complex, but evidence indicates that T cell-derived cytokines enhance the synthesis of matrix metalloproteinases (MMP) that contribute to mucosal ulceration and epithelial damage. In this study, we have examined the role of the T cell cytokine IL-21 in Hp-infected gastric mucosa and evaluated whether IL-21 regulates MMP production by gastric epithelial cells. We show that IL-21 is constitutively expressed in gastric mucosa and is more abundant in biopsy specimens and purified mucosal CD3(+) T cells from Hp-infected patients compared with normal patients and disease controls. We also demonstrate that IL-21R is expressed by primary gastric epithelial cells, as well as by the gastric epithelial cell lines AGS and MKN28. Consistently, AGS cells respond to IL-21 by increasing production of MMP-2 and MMP-9, but not MMP-1, MMP-3, MMP-7, or tissue inhibitors of MMP. Analysis of signaling pathways leading to MMP production reveals that IL-21 enhances NF-kappaB but not MAPK activation, and inhibition of NF-kappaB activation reduces IL-21-induced MMP-2 and MMP-9 production. Finally, we show that treatment of Hp-infected gastric explants with anti-IL-21 reduces epithelial cell-derived MMP-2 and MMP-9 production. These data indicate that IL-21 is overexpressed in Hp-infected gastric mucosa where it could contribute to increased epithelial gelatinase production.lld:pubmed
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pubmed-article:17442980pubmed:articleTitleIL-21 is highly produced in Helicobacter pylori-infected gastric mucosa and promotes gelatinases synthesis.lld:pubmed
pubmed-article:17442980pubmed:affiliationDepartment of Internal Medicine and Centre of Excellence for Genomic Risk Assessment in Multifactorial and Complex Diseases, University of Rome Tor Vergata, Rome, Italy.lld:pubmed
pubmed-article:17442980pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:17442980pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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