Prior Helicobacter pylori infection ameliorates Salmonella typhimurium-induced colitis: mucosal crosstalk between stomach and distal intestine.
Prior Helicobacter pylori infection ameliorates Salmonella typhimurium-induced colitis: mucosal crosstalk between stomach and distal intestine.
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DOI:
10.1002/ibd.21489
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发表时间:
2011-06
影响因子:
4.9
通讯作者:
Kao, John Y.
中科院分区:
文献类型:
--
作者:
Higgins, Peter D. R.;Johnson, Laura A.;Luther, Jay;Zhang, Min;Sauder, Kay L.;Blanco, Luz P.;Kao, John Y.
Helicobacter pylori infection is associated with a lower risk of chronic autoimmune diseases including IBD. H. pylori modulates the gastric immune response, decreasing the local inflammatory response to itself. In mice, chronic Salmonella typhimurium infection induces colitis similar to Crohn’s disease characterized by inflammation which progresses towards fibrosis. The aim of this study was to determine whether prior H. pylori infection acts at a distance to modulate the immune response of S. typhimurium-induced colitis. Mice were infected with the mouse-adapted strain of H. pylori (SS1), followed by infection with S. typhimurium. The effect of H. pylori on colitis was determined by gross pathology, histopathology, cytokine response, and development of fibrosis in the cecum. Gastritis and systemic immune response was measured in response to infection. H. pylori suppresses the Th17 response to S. typhimurium infection in the mouse cecum, but does not alter the Th2 or Treg response or the development of fibrosis. H. pylori infection induces IL-10 in the mesenteric lymph nodes, suggesting an extra-gastric mechanism for immunomodulation. H. pylori/S. typhimurium co-infection decreases inflammation in both the cecum and the stomach. This study demonstrates a potential mechanism for the negative association between H. pylori and IBD in humans. H. pylori represses the lower gastrointestinal tract Th17 response to bacterially induced colitis via extra-gastric immunomodulatory effects, illustrating immunological crosstalk between the upper and lower gastrointestinal tract.
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影响因子:
14.8
作者:
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通讯作者:
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影响因子:
158.5
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影响因子:
29.4
作者:
Rad, Roland;Brenner, Lena;Prinz, Christian
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Prinz, Christian
DOI:
10.1152/ajpgi.1999.276.6.g1317
发表时间:
1999-06-01
影响因子:
4.5
作者:
De Winter, H;Cheroutre, H;Kronenberg, M
通讯作者:
Kronenberg, M