Open AccessThe Capsule-Encoding viaB Locus Reduces Intestinal Inflammation by a Salmonella Pathogenicity Island 1-Independent Mechanism
Author(s) -
Takeshi Haneda,
Sebastian Winter,
Brian P. Butler,
Ronald P. Wilson,
Çaǧla Tükel,
Maria G. Winter,
Ivan Godinez,
Renée M. Tsolis,
Andreas J. Bäumler
Publication year - 2009
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.00172-09
Subject(s) - biology , salmonella enterica , microbiology and biotechnology , serotype , inflammation , salmonella , pathogenicity island , type three secretion system , locus (genetics) , cecum , secretion , salmonella typhi , immunology , enterobacteriaceae , virulence , bacteria , gene , escherichia coli , genetics , ecology , biochemistry
Salmonella enterica serotype Typhimurium elicits acute neutrophil influx in the human intestinal mucosa within 1 or 2 days after infection, resulting in inflammatory diarrhea. In contrast, no overt symptoms are observed within the first 1 or 2 weeks after infection withS. enterica serotype Typhi. Here we show that introduction of the capsule-encodingviaB locus of serotype Typhi reduced the ability of serotype Typhimurium to elicit acute intestinal inflammation in a streptomycin-pretreated mouse model. Serotype Typhimurium requires a functional invasion-associated type III secretion system (type III secretion system 1 [T3SS-1]) to elicit cecal inflammation within 48 h after infection of streptomycin-pretreated mice, and the presence of theviaB locus reduced its invasiveness for human intestinal epithelial cells in vitro. However, a reduced activity of T3SS-1 could not account for the ability of theviaB locus to attenuate cecal inflammation, because introduction of theviaB locus into an invasion-deficient serotype Typhimurium strain (invA mutant) resulted in a significant reduction of pathology and inflammatory cytokine expression in the cecum 5 days after infection of mice. We conclude that a T3SS-1-independent mechanism contributes to the ability of theviaB locus to reduce intestinal inflammation.