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Title:

The Salmonella pathogenicity island (SPI)-2 and SPI-1 type III secretion systems allow Salmonella serovar typhimurium to trigger colitis via MyD88-dependent and MyD88-independent mechanisms.

Document type:
Journal Article
Author(s):
Hapfelmeier, S; Stecher, B; Barthel, M; Kremer, M; Müller, AJ; Heikenwalder, M; Stallmach, T; Hensel, M; Pfeffer, K; Akira, S; Hardt, WD
Abstract:
Salmonella typhimurium can colonize the gut, invade intestinal tissues, and cause enterocolitis. In vitro studies suggest different mechanisms leading to mucosal inflammation, including 1) direct modulation of proinflammatory signaling by bacterial type III effector proteins and 2) disruption or penetration of the intestinal epithelium so that penetrating bacteria or bacterial products can trigger innate immunity (i.e., TLR signaling). We studied these mechanisms in vivo using streptomycin-pretr...     »
Journal title abbreviation:
J Immunol
Year:
2005
Journal volume:
174
Journal issue:
3
Pages contribution:
1675-85
Language:
eng
Pubmed ID:
http://view.ncbi.nlm.nih.gov/pubmed/15661931
Print-ISSN:
0022-1767
TUM Institution:
Institut für Allgemeine Pathologie und Pathologische Anatomie
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