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Merck

Salmonella Typhimurium exploits inflammation to its own advantage in piglets.

Frontiers in microbiology (2015-10-07)
Barbara Chirullo, Michele Pesciaroli, Rosanna Drumo, Jessica Ruggeri, Elisabetta Razzuoli, Claudia Pistoia, Paola Petrucci, Nicola Martinelli, Lucilla Cucco, Livia Moscati, Massimo Amadori, Chiara F Magistrali, Giovanni L Alborali, Paolo Pasquali
RESUMEN

Salmonella Typhimurium (S. Typhimurium) is responsible for foodborne zoonotic infections that, in humans, induce self-limiting gastroenteritis. The aim of this study was to evaluate whether the wild-type strain S. Typhimurium (STM14028) is able to exploit inflammation fostering an active infection. Due to the similarity between human and porcine diseases induced by S. Typhimurium, we used piglets as a model for salmonellosis and gastrointestinal research. This study showed that STM14028 is able to efficiently colonize in vitro porcine mono-macrophages and intestinal columnar epithelial (IPEC-J2) cells, and that the colonization significantly increases with LPS pre-treatment. This increase was then reversed by inhibiting the LPS stimulation through LPS antagonist, confirming an active role of LPS stimulation in STM14028-intracellular colonization. Moreover, LPS in vivo treatment increased cytokines blood level and body temperature at 4 h post infection, which is consistent with an acute inflammatory stimulus, capable to influence the colonization of STM14028 in different organs and tissues. The present study proves for the first time that in acute enteric salmonellosis, S. Typhimurium exploits inflammation for its benefit in piglets.

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Sigma-Aldrich
Lipopolysaccharides from Salmonella enterica serotype typhimurium, purified by gel-filtration chromatography