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- Bäckhed, Fredrik, 1973, et al.
(author)
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Gastric mucosal recognition of Helicobacter pylori is independent of Toll-like receptor 4
- 2003
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In: J Infect Dis. - 0022-1899. ; 187:5, s. 829-36
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Journal article (peer-reviewed)abstract
- Little is known about the interactions between Helicobacter pylori, which specializes in colonizing the mucin layer that covers the gastric mucosa, and primary gastric epithelial cells. The expression pattern of Toll-like receptors (TLRs) in primary gastric epithelial cells and cell lines was compared. Primary cells did not express TLR4, whereas all cell lines expressed a nonsignaling form of TLR4. Because other cells within the mucosa expressed TLR4, it was next investigated whether H. pylori can be recognized by TLR4--they cannot. Moreover, H. pylori infection of primary cells induced a regulated production of interleukin (IL)-6, IL-8, and tumor necrosis factor-alpha, whereas infection of cell lines only resulted in IL-8 production. The cytokine production in all cell types was strictly cag dependent. These findings indicate that, although the epithelium is important in directing the immune response against H. pylori infections, the response is independent of TLR4.
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- Bäckhed, Fredrik, 1973, et al.
(author)
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Helicobacter pylori infection induces interleukin-8 receptor expression in the human gastric epithelium
- 2003
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In: Infect Immun. - 0019-9567. ; 71:6, s. 3357-60
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Journal article (peer-reviewed)abstract
- The gastric pathogen Helicobacter pylori is known to activate multiple proinflammatory signaling pathways in epithelial cells. In this study, we addressed the question of whether expression of the interleukin-8 receptors IL-8RA (CXCR1) and IL-8RB (CXCR2) is upregulated in H. pylori-infected human gastric biopsy samples. Biopsy samples from patients infected with H. pylori strains harboring the cag pathogenicity island (PAI) expressed larger amounts of both receptors. In addition, IL-8RB expression was induced in the gastric epithelial cell line AGS upon infection with a clinical isolate containing the cag PAI, while a strain lacking the cag PAI did not. Our finding suggests that gastric epithelial cells express IL-8R in response to H. pylori infection.
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- Soderblom, T, et al.
(author)
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Bacterial protein toxins and inflammation
- 2003
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In: Scandinavian journal of infectious diseases. - : Informa UK Limited. - 0036-5548 .- 1651-1980. ; 35:9, s. 628-631
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Journal article (peer-reviewed)
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