Dana Elhadad, Michael McClelland, Galia Rahav, and Ohad Gal-Mor.
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 (39-42°C) Salmonella enterica serovars Typhi, Paratyphi A and Sendai significantly attenuate their motility, epithelial cell invasion and uptake by macrophages. Under these fever-like conditions, the residual epithelial cell invasion of S. Paratyphi A occurs in a T3SS-1-independent manner and results in restrained disruption of epithelium integrity. The impaired motility and invasion are associated with downregulation of Type Three Secretion System (T3SS)-1 genes and classes II and III, (but not I) of the flagella-chemotaxis regulon. In contrast, we demonstrate upregulation of SPI-2 genes 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 non-typhoidal salmonellae.
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