Experimental Yersinia enterocolitica infection in rodents: A model for human yersiniosis

Abstract

enterocolitica infection in rodents: A model for human yersiniosis. APMIS 101: 417429, 1993. Yersiniu enterocoliticu infection in humans causes a broad spectrum of diseases ranging from acute bowel disease to extraintestinal manifestations such as reactive arthritis, erythema nodosum and uveitis. During the last decade a fascinating part of the molecular biology of the pathogenicity of human pathogenic Yersinia species has been unraveled. Pathogenicity factors such as protein tyrosine phosphatase, protein kinase, thrombin-and collagen-binding factors have been identified and characterized on the molecular level. In contrast to many animal models for human enteropathogenic microorganisms, experimental Y enterocoliticu infection in rodents resembles yersiniosis in humans and thus offers extraordinary opportunities to study the sequential steps of the infectious process. Rabbits are suitable animals in which to study Yersinia-induced enteritis (enterotoxin-mediated) and the humoral immune response after oral infection. The role of Peyer's patches (PP) in the entry of enteropathogenic Yersinia species has been elucidated in mice and rabbits. M cells are probably the primary target cells of invading Yersiniae. Surprisingly, after penetration of the mucosal epithelial cell layer Yersinia bacilli were visualized to be exclusively extracellular in PP tissue. Obviously neutrophils within PP were unable to phagocytize the invading microorganisms. Presently, it is not clear how the microorganisms disseminate from PP into lymph nodes, spleen, liver and lung of mice where they form abscesses and granuloma-like lesions. Immunohistologically the involvement of macrophages and T cells could be demonstrated in Yersinia-induced lesions of mice. Direct evidence for the role of T cells and cytokine-activated macrophages in the host defense reaction against a primary Yersinia infection in mice could be obtained from experiments including adoptive transfer of Yersinia-specific T cells and in vivo neutralization of TNF-alpha and IFN-gamma. The experimental rat model turned out to be a suitable model for studying Yersinia-induced aseptic arthritis. Lewisand SHR rats proved to be arthritis-susceptible. Arthritogenicity of Yersinia for rats appeared to be restricted to I: enterocoliticu of serotype 08 and correlated with the virulence potential of this serotype. Surprisingly, expression of YadA, the collagen-binding factor, was not necessary for arthritis induction. A close association between both susceptibility to arthritis induction and Yersinia infection could be demonstrated in various rat strains. Depletion of alpha/beta T-cell receptor (crp-TCR)-positive T cells by treatment with ap-TCR-specific antibody revealed that T cells were required for clearance of the pathogen. However, in contrast to e.g. adjuvant arthritis, Yersinia-induced arthritis in Lewis rats was not affected by T-cell depletion. Thus, we expect significant differences between the pathomechanisms of Yersinia-triggered arthritis and antigen-induced arthritis in Le...

Association between clinical presentation, biogroups and virulence attributes ofYersinia enterocoliticastrains in human diarrhoeal disease

“…However, present mouse and rat models focus on systemic disease caused by yersiniae, i.e. septicaemic infections and post-infectious arthritis [24]. No simple animal models which entirely reproduce human intestinal disease due to Y.…”

Uptake of Killed Yersinia enterocolitica by Pseudopodia of M Cells in the Peyers' Patches of the Murine Small Intestines.

“…Although there are some reports on the involvement of M cells in the initial step of the infection with enteric pathogens [1][2][3][4][5], the formation of the pseudopodium as big as that demostrated in the present study is not known. Therefore, the pseudopodia may have been developed specifically for uptake of the killed bacteria.…”

“…A thinner pseudopodium was observed in M It has been shown that microfold (M) cells in the epithelium of the Peyer's patches dome region are involved in the initial stage of the invasion of enteropathogens [2,8,11]. An association of M cells with the intestinal invasion of Yersinia known as an agent of human gastroenteritis is known [1,[3][4][5]. The mechanism of the invasion of these pathogens into the M cells, however, is still obscure.…”

Experimental kinetics of infection induced by Yersinia pseudotuberculosis isolated from stock animals

“…Several studies have highlighted differences in the resistance of various mouse strains to intravenous infection with Y. enterocolitica. (Hancock et al 1986, Heesemann et al 1993, Autenrieth et al 1994. By the other hand, Handley et al (2004) working with different strains of inbred mice related that the animals presented no differences in 50% lethal dose ( LD 50 ) following oral infection with Y. enterocolitica.…”

“…The latter has been well documented in Y. enterocolitica (Quan et al 1974, Carter & Collins 1974, Alonso et al 1975, 1978, Une 1977, Falcão et al 1984, Apfel & Noleto 1991, Bauab & Falcão 1991, Heesemann et al 1993. However in Y. pseudotuberculosis, only a few studies have shown in vivo infection, and the kinetics has not been studied.…”