A1 Refereed original research article in a scientific journal

Persistence of Yersinia antigens in peripheral blood cells from patients with Yersinia enterocolitica O : 3 infection with or without reactive arthritis




AuthorsGranfors K, Merilahti-Palo R, Luukkainen R, Mottonen T, Lahesmaa R, Probst P, Marker-Hermann E, Toivanen P

PublisherLIPPINCOTT WILLIAMS & WILKINS

Publication year1998

JournalArthritis and Rheumatism

Journal name in sourceARTHRITIS AND RHEUMATISM

Journal acronymARTHRITIS RHEUM

Volume41

Issue5

First page 855

Last page862

Number of pages8

ISSN0004-3591

DOIhttps://doi.org/10.1002/1529-0131(199805)41:5<855::AID-ART12>3.0.CO;2-J


Abstract
Objective, To assess the persistence of bacterial antigens in peripheral blood cells from patients with Yersinia enterocolitica O:3-triggered reactive arthritis (ReA).Methods. Peripheral blood samples were obtained from 20 patients with Y enterocolitica O:3 infection (11 with ReA and 9 without). These samples were studied by immunochemical techniques for the presence of Yersinia antigens at the beginning of infection and up to 4 Sears thereafter. Synovial fluid samples from 6 of the 11 ReA patients were also studied.Results. The Yersinia antigens lipopolysaccharide and heat-shock protein (HSP) were detected in peripheral blood mononuclear cells and polymorphonuclear phagocytes from all patients studied at the early phase of the disease. They were also found in the synovial fluid cells of patients with Yersinia-triggered ReA. At 4 years after the onset of infection, these bacterial antigens were still detected in the peripheral blood cells of most of the ReA patients studied.Conclusion. This study has, for the first time, directly demonstrated that bacterial antigens persist for a long time in patients who develop ReA after Y enterocolitica O:3 infection. The finding of bacterial HSP in synovial fluid cells could provide a link to the pathogenesis of ReA since T cell responses of synovial cells have been shown to be directed against that structure. A close similarity between the bacterial and host HSP might contribute to the development of the relatively common, chronic form of this complication.



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