title: Host immune status influences the development of attaching and effacing lesions in weaned pigs.
abstract: Attaching and effacing Escherichia coli (AEEC) has been associated with naturally occurring attaching and effacing (A/E) lesions in weaned pigs, and although A/E lesions have been experimentally reproduced in newborn piglets, such lesions have been much more difficult to induce in older conventional pigs. Hence, the aim of this study was to examine the effect of oral administration of dexamethasone on the development of A/E lesions in weaned pigs challenged with a porcine enteropathogenic E. coli (PEPEC) strain and to investigate the involvement of local intestinal cytokine response. Dexamethasone, given orally at a dosage of 3 mg kg of body weight(-1), significantly enhanced both the colonization of the challenge strain and the prevalence of foci of intimately adherent bacteria, resulting in extensive A/E lesions in the ileum, cecum, and colon of challenged pigs. We also confirmed the expression of both intimin and Tir by PEPEC strain ECL1001 in A/E lesions in vivo, which is, to our knowledge, the first report of the involvement of the latter proteins in any AEEC infections in vivo. Moreover, semiquantitative reverse transcription-PCR demonstrated that interleukin 1beta (IL-1beta), IL-6, IL-8, and, to a lesser extent, IL-12p40 are significantly upregulated in the ileum following challenge with strain ECL1001, whereas dexamethasone blocks such upregulation. Taken together, our results strongly suggested that host immune status influences the development of A/E lesions in weaned pigs, and it appears that IL-1beta, IL-6, IL-8, and, to a lesser extent, IL-12p40 are expressed during infection of weaned pigs by PEPEC and may contribute to the natural resistance of the host against PEPEC infection.
authors.affiliation: Groupe de recherche sur les maladies infectieuses du porc, Faculté de médecine vétérinaire, Université de Montréal, Québec, Canada.
authors.forename: Francis
authors.initials: F
authors.lastname: Girard
authors.forename: Isabelle P
authors.initials: IP
authors.lastname: Oswald
authors.forename: Ionélia
authors.initials: I
authors.lastname: Taranu
authors.forename: Pierre
authors.initials: P
authors.lastname: Hélie
authors.forename: Greg D
authors.initials: GD
authors.lastname: Appleyard
authors.forename: Josée
authors.initials: J
authors.lastname: Harel
authors.forename: John M
authors.initials: JM
authors.lastname: Fairbrother
mesh_terms: D018829:Adhesins, Bacterial / Q000276:immunology; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001422:Bacterial Adhesion / Q000276:immunology*; D016207:Cytokines / Q000378:metabolism; D003907:Dexamethasone / Q000494:pharmacology; D004926:Escherichia coli / Q000276:immunology; D004927:Escherichia coli Infections / Q000276:immunology* / Q000382:microbiology / Q000662:veterinary*; D029968:Escherichia coli Proteins / Q000276:immunology; D007079:Ileitis / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology / Q000662:veterinary*; D007113:Immunity, Innate; D015151:Immunoblotting / Q000662:veterinary; D007249:Inflammation / Q000188:drug therapy / Q000276:immunology / Q000662:veterinary; D011956:Receptors, Cell Surface / Q000276:immunology; D013552:Swine; D013553:Swine Diseases / Q000276:immunology*; D014886:Weaning
chemical_list: D018829:Adhesins, Bacterial; D000893:Anti-Inflammatory Agents; D016207:Cytokines; D029968:Escherichia coli Proteins; D011956:Receptors, Cell Surface; C109287:Tir protein, E coli; C073819:eaeA protein, E coli; D003907:Dexamethasone