期刊
JOURNAL OF INFECTIOUS DISEASES
卷 212, 期 1, 页码 147-156出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiu663
关键词
enteric fever; pyrexia; paratyphoid; Salmonella; pathogenicity; motility; flagella; invasion
资金
- German-Israeli Foundation for Scientific Research and Development [1096-39.11/2010]
- Israel Science Foundation [999/14]
- National Institutes of Health [HHSN272200900040C, AI039557 AI052237, AI073971, AI075093, AI077645 AI083646, USDA 2009-03579, 2011-67017-30127]
- Binational Agricultural Research and Development Fund
- Center for Produce Safety
Human infection with typhoidal Salmonella serovars causes a febrile systemic disease, termed enteric fever. Here we establish that in response to a temperature equivalent to fever (39 degrees C-42 degrees C) Salmonella enterica serovars Typhi, Paratyphi A, and Sendai significantly attenuate their motility, epithelial cell invasion, and uptake by macrophages. Under these feverlike conditions, the residual epithelial cell invasion of S. Paratyphi A occurs in a type III secretion system (T3SS) 1-independent manner and results in restrained disruption of epithelium integrity. The impaired motility and invasion are associated with down-regulation of T3SS-1 genes and class II and III (but not I) of the flagella-chemotaxis regulon. In contrast, we demonstrate up-regulation of particular Salmonella pathogenicity island 2 genes (especially spiC) and increased intraepithelial growth in a T3SS-2-dependent manner. These results indicate that elevated physiological temperature is a novel cue controlling virulence phenotypes in typhoidal serovars, which is likely to play a role in the distinct clinical manifestations elicited by typhoidal and nontyphoidal salmonellae.
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