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Publication : Nod1 and Nod2 regulation of inflammation in the Salmonella colitis model.

First Author  Geddes K Year  2010
Journal  Infect Immun Volume  78
Issue  12 Pages  5107-15
PubMed ID  20921147 Mgi Jnum  J:166072
Mgi Id  MGI:4839677 Doi  10.1128/IAI.00759-10
Citation  Geddes K, et al. (2010) Nod1 and nod2 regulation of inflammation in the salmonella colitis model. Infect Immun 78(12):5107-15
abstractText  The pattern recognition molecules Nod1 and Nod2 play important roles in intestinal homeostasis; however, how these proteins impact on the development of inflammation during bacterial colitis has not been examined. In the streptomycin-treated mouse model of Salmonella colitis, we found that mice deficient for both Nod1 and Nod2 had attenuated inflammatory pathology, reduced levels of inflammatory cytokines, and increased colonization of the mucosal tissue. Nod1 and Nod2 from both hematopoietic and nonhematopoietic sources contributed to the pathology, and all phenotypes were recapitulated in mice deficient for the signaling adaptor protein Rip2. However, the influence of Rip2 was strictly dependent on infection conditions that favored expression of the Salmonella pathogenicity island 2 (SPI-2) type III secretion system (TTSS), as Rip2 was dispensable for inflammation when mice were infected with bacteria grown under conditions that promoted expression of the SPI-1 TTSS. Thus, Nod1 and Nod2 can modulate inflammation and mediate efficient clearance of bacteria from the mucosal tissue during Salmonella colitis, but their role is dependent on the expression of the SPI-2 TTSS.
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