Development of an experimental animal model for reactive arthritis induced by Yersinia enterocolitica infection

Hill, Jeri L.; Yu, David Tak Yan

doi:10.1128/iai.55.3.721-726.1987

Cited by 78 publications

(22 citation statements)

References 11 publications

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“…It is well established that Y. enterocolitica is a relatively common microorganism involved in the aetiology of reactive arthritis. The most frequently occurring human arthritogenic serotype of Y. enterocolitica is 0:3, which has low virulence for mice and is found to be non-arthritogenic for rats (Hill and Yu, 1987). Surprisingly, the mouse virulent Y. enterocolitica serotype 0:8, which is rarely described as being arthritogenic in humans, proved to be arthritogenic in Lewis rats (Toivanen et al, 1986).…”

Section: Discussionmentioning

confidence: 99%

“…When aiming to study the pathogenesis of Yersinia-associated arthritis, an appropriate animal model for Yersinia-triggered arthritis is required. Aseptic arthritis in rats is induced by experimental intravenous infection with the highly pathogenic Y. enterocolitica serotype 0:8 (Toivanen et al, 1986;Hill and Yu, 1987). Toyos et al (1990) have shown that Y. enterocolitica 0:3 is experimentally arthritogenic for mice after oral inoculation.…”

Section: Introductionmentioning

confidence: 99%

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Arthritis after Experimental Infection with Yersinia enterocolitica 0:3 in Rabbits

et al. 2001

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Arthritis in rabbits was caused after experimental oral infection with Yersinia enterocolitica (serotype 0:3, biotype 4, pYV+). Clinical and laboratory signs, bacterial dissemination to the viscera, immune response and morphological findings were studied from day 1 to day 40 post-infection (p.i.). Augmentation of body temperature and erythrocyte sedimentation rate occurred on day 1, and on day 8 p.i. was accompanied by leucopenia. The number of alveolar macrophages was increased up to the 15th day p.i., in contrast to peritoneal macrophage numbers. Extensive bacterial colonization of the internal organs was detected at necropsy until the end of the experiment. Analysis of the cell immune response revealed activation of B cells in peripheral blood, spleen and thymus as well as augmentation of T-cell number in the lymphoid organs examined on days 15, 28 and 40 p.i. Histological changes typical of a generalized infection, such as purulent meningoencephalitis, catarrhal pneumonia and lymphadenitis, were observed. Clinical and morphological manifestations of arthritis were also established. The results obtained show that Y. enterocolitica (serotype 0:3, pYV+) induces a generalized, non-lethal infection in Chinchilla rabbits, complicated by arthritis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Arthritis after Experimental Infection with Yersinia enterocolitica 0:3 in Rabbits

et al. 2001

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“…in Lewis rats by intravenous administration of lo4 to lo5 live I: enterocolitica of serotype 0 8 (48). The course of the disease resembled that of Yersinia-reactive arthritis in humans.…”

Section: H I L L and Yu Were Able To Elicit Aseptic Arthritismentioning

confidence: 91%

“…Previously, two research groups succeeded in inducing arthritis in rats by experimental infection with Y enterocolitica (48,83).…”

Section: Yrrsiniu-induced Arthritis In Experimentally Infected Rutsmentioning

confidence: 99%

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

Heesemann

Gaede

Autenrieth

1993

APMIS

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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...

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“…The possibilities of other mechanisms or contributing factors, mentioned above, further complicate the pathological situation in the spondyloarthropathies. The recently reported animal model of reactive arthritis in response to yersinia infection should make possible certain enlightening studies on the participating mechanism(s) in enteric bacteria-induced ReA (Hill & Yu 1987). Another potentially fruitful area for future research is the further analysis of events within the affected joints.…”

Section: Other Possible M E C H a N I S M S / C O N T R I B U T I N Gmentioning

confidence: 99%

Foodborne enterobacterial pathogens and rheumatoid disease

Bunning

Raybourne

Archer

1988

Journal of Applied Bacteriology

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Development of an experimental animal model for reactive arthritis induced by Yersinia enterocolitica infection

Cited by 78 publications

References 11 publications

Arthritis after Experimental Infection with Yersinia enterocolitica 0:3 in Rabbits

Arthritis after Experimental Infection with Yersinia enterocolitica 0:3 in Rabbits

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

Foodborne enterobacterial pathogens and rheumatoid disease

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