The inflammatory cytokine tumor necrosis factor modulates the expression of <it>Salmonella </it>typhimurium effector proteins
<p>Abstract</p> <p>Tumor necrosis factor α (TNF-α)is a host inflammatory factor. Bacteria increase TNF-α expression in a variety of human diseases including infectious diseases, inflammatory bowel diseases, and cancer. It is unknown, however, how TNF-α directly modulates bacterial...
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| Main Authors: | , , , |
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| Format: | Book |
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BMC,
2010-08-01T00:00:00Z.
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| Online Access: | Connect to this object online. |
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| Summary: | <p>Abstract</p> <p>Tumor necrosis factor α (TNF-α)is a host inflammatory factor. Bacteria increase TNF-α expression in a variety of human diseases including infectious diseases, inflammatory bowel diseases, and cancer. It is unknown, however, how TNF-α directly modulates bacterial protein expression during intestinal infection and chronic inflammation. In the current study, we hypothesize that <it>Salmonella </it>typhimurium senses TNF-α and show that TNF-α treatment modulates <it>Salmonella </it>virulent proteins (called effectors), thus changing the host-bacterial interaction in intestinal epithelial cells. We investigated the expression of 23 <it>Salmonella </it>effectors after TNF-α exposure. We found that TNF-α treatment led to differential effector expression: effector SipA was increased by TNF-α treatment, whereas the expression levels of other effectors, including gogB and spvB, decreased in the presence of TNF-α. We verified the protein expression of <it>Salmonella </it>effectors AvrA and SipA by Western blots. Furthermore, we used intestinal epithelial cells as our experimental model to explore the response of human intestinal cells to TNF-α pretreated <it>Salmonella</it>. More bacterial invasion was found in host cells colonized with <it>Salmonella </it>strains pretreated with TNF-α compared to <it>Salmonella </it>without TNF-α treatment. TNF-α pretreated <it>Salmonella </it>induced higher proinflammatory JNK signalling responses compared to the <it>Salmonella </it>strains without TNF-α exposure. Exposure to TNF-α made <it>Salmonella </it>to induce more inflammatory cytokine IL-8 in intestinal epithelial cells. JNK inhibitor treatment was able to suppress the effects of TNF-pretreated-<it>Salmonella </it>in enhancing expressions of phosphorylated-JNK and c-jun and secretion of IL-8. Overall, our study provides new insights into <it>Salmonella</it>-host interactions in intestinal inflammation.</p> |
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| Item Description: | 10.1186/1476-9255-7-42 1476-9255 |