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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.
Hapfelmeier S, Stecher B, Barthel M, Kremer M, Müller AJ, Heikenwalder M, Stallmach T, Hensel M, Pfeffer K, Akira S, Hardt WD. Hapfelmeier S, et al. Among authors: kremer m. J Immunol. 2005 Feb 1;174(3):1675-85. doi: 10.4049/jimmunol.174.3.1675. J Immunol. 2005. PMID: 15661931
Motility allows S. Typhimurium to benefit from the mucosal defence.
Stecher B, Barthel M, Schlumberger MC, Haberli L, Rabsch W, Kremer M, Hardt WD. Stecher B, et al. Among authors: kremer m. Cell Microbiol. 2008 May;10(5):1166-80. doi: 10.1111/j.1462-5822.2008.01118.x. Epub 2008 Jan 30. Cell Microbiol. 2008. PMID: 18241212
Microbe sampling by mucosal dendritic cells is a discrete, MyD88-independent step in DeltainvG S. Typhimurium colitis.
Hapfelmeier S, Müller AJ, Stecher B, Kaiser P, Barthel M, Endt K, Eberhard M, Robbiani R, Jacobi CA, Heikenwalder M, Kirschning C, Jung S, Stallmach T, Kremer M, Hardt WD. Hapfelmeier S, et al. Among authors: kremer m. J Exp Med. 2008 Feb 18;205(2):437-50. doi: 10.1084/jem.20070633. Epub 2008 Feb 11. J Exp Med. 2008. PMID: 18268033 Free PMC article.
588 results