July 22, 2005

Francis Girard, EcL PhD student, recently successfully defended his doctoral thesis, entitled "Étude de la pathogenèse des infections à Escherichia coli attachants et effaçants chez le porc". Part of this work will be published as two articles in the September edition of Infection and Immunity. These articles are entitled "Host immune status influences the development of attaching and effacing lesions in weaned pigs" and "Interaction of enteropathogenic and Shiga-toxin producing Escherichia coli with porcine intestinal mucosa: Role of Intimin and Tir in adherence" (Infect Immun Vol 73).

 

Girard F, Oswald IP, Taranu I, Helie P, Appleyard GD, Harel J and Fairbrother JM (2005). Host immune status influences the development of attaching and effacing lesions in weaned pigs. Infection and Immunity 73: 5514-5523.

Abstract (PubMed)

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.

 

Girard F, Batisson I, Frankel GM, Harel J and Fairbrother JM (2005). Interaction of enteropathogenic and Shiga-toxin producing Escherichia coli with porcine intestinal mucosa: Role of Intimin and Tir in adherence. Infection and Immunity 73: 6005-6016.

Abstract (PubMed)

The ileal in vitro organ culture (IVOC) model using tissues originating from colostrum-deprived newborn piglets has proven to be an effective way to study the attaching and effacing (A/E) phenotype of porcine enteropathogenic Escherichia coli (EPEC) ex vivo. The aim of this study was to investigate the role of intimin subtype and Tir in the adherence of EPEC and Shiga-toxin-producing E. coli (STEC), isolated from different animal species, to porcine intestinal IVOC. Moreover, the role of intimin in Tir-independent adherence of the human EPEC strain E2348/69 was investigated using intimin and Tir-deficient derivatives. Our results demonstrated that A/E E. coli strains (AEEC) from various animal species and humans induce the A/E phenotype in porcine ileal IVOC and that intimin subtype influences intestinal adherence and tropism of AEEC strains. We also showed that a tir mutant of EPEC strain E2348/69 demonstrates close adherence to the epithelial cells of porcine ileal IVOC segments, with microvillous effacement but with no evidence of actin polymerization or pedestal formation, and that intimin seems to be involved in this phenotype. Overall, this study provides further evidence for the existence of one or more host-cell-encoded intimin receptor(s) in the pig gut.

 

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