ShiA Abrogates the Innate T-Cell Response to Shigella flexneri Infection

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ShiA abrogates the innate T-cell response to Shigella flexneri infection.

Shigella spp. are the causative agent of bacillary dysentery. Infection results in acute colonic injury due to the host inflammatory response. The mediators of the damage, infiltrating polymorphonuclear leukocytes (PMN), also resolve the infection. Shigella flexneri's virulence effectors are encoded on its large virulence plasmid and on pathogenicity islands in the chromosome. The SHI-2 pathoge...

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Roles for T and NK cells in the innate immune response to Shigella flexneri.

Shigella flexneri, an enteroinvasive Gram-negative bacterium, is responsible for the worldwide endemic form of bacillary dysentery. The host response to primary infection is characterized by the induction of an acute inflammation, which is accompanied by polymorphonuclear cell (PMN) infiltration, resulting in massive destruction of the colonic mucosa. However, PMN play a major role in the recov...

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T-lymphocyte clones responsive to Shigella flexneri.

T lymphocytes from a patient with Shigella flexneri dysentery and postdysenteric reactive arthritis were cloned by limiting dilution with recombinant interleukin-2 and a strain of S. flexneri different from that which had infected her. Five of eight clones produced proliferated in response to the shigellae used to generate the clones. The response required irradiated syngeneic blood mononuclear...

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Fulminating encephalopathy associated with Shigella flexneri infection.

Three cases of rapidly fatal encephalopathy associated with Shigella flexneri infection are reported. There was a lack of severe intestinal involvement and absence of metabolic derangement. In all 3 patients, areas of necrosis were present throughout the brains; and in one case pontine haemorrhages and demyelination were seen. This report supports the evidence of a particular neurotoxic effect ...

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ژورنال

عنوان ژورنال: Infection and Immunity

سال: 2006

ISSN: 0019-9567,1098-5522

DOI: 10.1128/iai.74.4.2317-2327.2006