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Molecular basis of Salmonella ‐induced enteritis
Author(s) -
Wallis Timothy S.,
Galyov Edouard E.
Publication year - 2000
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.2000.01892.x
Subject(s) - virulence , biology , salmonella , pathogenicity island , effector , secretion , microbiology and biotechnology , enteritis , pathogenesis , type three secretion system , typhoid fever , enterobacteriaceae , chromosomal translocation , gene , bacteria , immunology , genetics , escherichia coli , biochemistry
Salmonella pathogenesis is a complex and multifactorial phenomenon. Many genes required for full virulence in mice have been identified, but only a few of these have been shown to be necessary for the induction of enteritis. Likewise, at least some of the Salmonella virulence factors affecting enteritis do not appear to be required for infection of systemic sites in mice. This suggests that subsets of virulence genes influence distinct aspects of Salmonella pathogenesis. Recently, considerable progress has been made in characterizing the virulence mechanisms influencing enteritis caused by non‐typhoid Salmonella spp. The Salmonella pathogenicity island‐1‐encoded type III secretion system mediates the translocation of secreted effector proteins into target epithelial cells. These effector proteins are key virulence factors required for Salmonella intestinal invasion and the induction of fluid secretion and inflammatory responses.