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• W2153027687 endingPage "6953" @default.
• W2153027687 startingPage "6943" @default.
• W2153027687 abstract "ABSTRACT Salmonella encounters various stresses in the environment and in the host during infection. The effects of cold (5°C, 48 h), peroxide (5 mM H 2 O 2 , 5 h) and acid stress (pH 4.0, 90 min) were tested on pathogenicity of Salmonella . Prior exposure of Salmonella to cold stress significantly ( P < 0.05) increased adhesion and invasion of cultured intestinal epithelial (Caco-2) cells. This increased Salmonella -host cell association was also correlated with significant induction of several virulence-associated genes, implying an increased potential of cold-stressed Salmonella to cause an infection. In Caco-2 cells infected with cold-stressed Salmonella , genes involved in the electron transfer chain were significantly induced, but no simultaneous significant increase in expression of antioxidant genes that neutralize the effect of superoxide radicals or reactive oxygen species was observed. Increased production of caspase 9 and caspase 3/7 was confirmed during host cell infection with cold-stressed Salmonella . Further, a prophage gene, STM2699 , induced in cold-stressed Salmonella and a spectrin gene, SPTAN1, induced in Salmonella -infected intestinal epithelial cells were found to have a significant contribution in increased adhesion and invasion of cold-stressed Salmonella in epithelial cells." @default.
• W2153027687 created "2016-06-24" @default.
• W2153027687 creator A5021167791 @default.
• W2153027687 creator A5076012964 @default.
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• W2153027687 date "2014-11-15" @default.
• W2153027687 modified "2023-09-23" @default.
• W2153027687 title "Genetic Mechanisms Underlying the Pathogenicity of Cold-Stressed Salmonella enterica Serovar Typhimurium in Cultured Intestinal Epithelial Cells" @default.
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• W2153027687 doi "https://doi.org/10.1128/aem.01994-14" @default.
• W2153027687 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4249018" @default.
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• W2153027687 hasPublicationYear "2014" @default.
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