title: Lipopolysaccharide-induced biliary factors enhance invasion of Salmonella enteritidis in a rat model.
abstract: In this study, the role of the hepatobiliary system in the early pathogenesis of Salmonella enteritidis infection was investigated in a rat model. Intravenous (i.v.) challenge with lipopolysaccharide (LPS) has previously been shown to enhance the translocation of normal gut flora. We first confirmed that LPS can similarly promote the invasion of S. enteritidis. Oral infection of outbred Australian Albino Wistar rats with 10(6) to 10(7) CFU of S. enteritidis led to widespread tissue invasion after days. If animals were similarly challenged after intravenous administration of S. enteritidis LPS (3 to 900 microg/kg of body weight), significant invasion of the livers and mesenteric lymph nodes (MLN) occurred within 24 h, with invasion of the liver increasing in a dose-dependent fashion (P < 0.01). If bile was prevented from reaching the intestine by bile duct ligation or cannulation, bacterial invasion of the liver and MLN was almost totally abrogated (P < 0.001). As i.v. challenge with LPS could induce the delivery of inflammatory mediators into the bile, biliary tumor necrosis factor alpha (TNF-alpha) concentrations were measured by bioassay. Biliary concentrations of TNF-alpha rose shortly after LPS challenge, peaked with a mean concentration of 27.0 ng/ml at around 1 h postchallenge, and returned to baseline levels (3.1 ng/ml) after 2.5 h. Although TNF-alpha cannot be directly implicated in the invasion process, we conclude that the invasiveness of the enteric pathogen S. enteritidis is enhanced by the presence of LPS in the blood and that this enhanced invasion is at least in part a consequence of the delivery of inflammatory mediators to the gastrointestinal tract by the hepatobiliary system.
authors.affiliation: School of Microbiology and Immunology, University of New South Wales, Australia. a.islam@unsw.edu.au
authors.forename: A F
authors.initials: AF
authors.lastname: Islam
authors.forename: N D
authors.initials: ND
authors.lastname: Moss
authors.forename: Y
authors.initials: Y
authors.lastname: Dai
authors.forename: M S
authors.initials: MS
authors.lastname: Smith
authors.forename: A M
authors.initials: AM
authors.lastname: Collins
authors.forename: G D
authors.initials: GD
authors.lastname: Jackson
mesh_terms: D000818:Animals; D001646:Bile / Q000378:metabolism; D001659:Biliary Tract / Q000187:drug effects* / Q000503:physiopathology*; D004195:Disease Models, Animal; D008070:Lipopolysaccharides / Q000633:toxicity*; D008099:Liver / Q000382:microbiology; D008198:Lymph Nodes / Q000382:microbiology; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D012481:Salmonella Infections, Animal / Q000209:etiology* / Q000382:microbiology; D012477:Salmonella enteritidis / Q000302:isolation & purification / Q000472:pathogenicity; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha