New arthritis immunology study findings have been published by scientists at National University
2007 MAY 28 -- Researchers detail in "Role of TNFRp55 in Yersinia enterocolitica O:3-induced arthritis: triggering bacterial antigens and articular immune response," new data in arthritis. According to recent research published in the journal Rheumatology, "The pathogenesis of reactive arthritis (ReA), an aseptic synovitis that follows an extra-articular infection, is incompletely known. We studied the impact of tumor necrosis factor receptor (TNFR) p55 deficiency on the progression to ReA after oral Yersinia enterocolitica O:3 infection, the Yersinia antigens triggering articular inflammation and a possible articular TNFRp55-mediated mechanism that protects against ReA." "Wild-type C57BL/6 and TNFRp55-/-mice were orogastrically infected with Y. enterocolitica O:3 and monitored for survival and arthritis development. The bacterial load was determined in mesenteric lymph nodes (MLNs), the spleen and joints. Interferon (IFN)-gamma, TNF-alpha and IL-10 mRNA expression in MLN and joints were analysed by reverse transcription-polymerase chain reaction (RT-PCR). Articular antibodies to Yersinia antigens, TNF-alpha protein and nitric oxide (NO) levels were assessed. Acute arthritis was evaluated after joint injection of Yersinia antigens. The survival rate was 60% in TNFRp55-/-mice. They showed impaired bacterial clearance in MLN, the spleen and joints, and excessive mRNA expression of pro-inflammatory cytokines in MLN. Clinical and histological examinations revealed that TNFRp55-/-mice developed severe arthritis. Moreover, augmented articular outer membrane protein (OMP)-specific antibodies and TNF-alpha but impaired NO levels were detected in TNFRp55-/-mice. Synovial inflammatory response was detected by joint OMP injection. TNFRp55-mediated immune mechanisms prevent ReA development after oral infection with Y. enterocolitica O:3. Yersinia OMPs are the relevant antigens triggering ReA. NO induction through TNFRp55 signalling could have a local antibacterial function to prevent ReA," wrote Genaro M.S. Di and colleagues, National University. The researchers concluded: "This study could contribute to ReA-specific therapeutic studies." Di and colleagues published their study in Rheumatology (Role of TNFRp55 in Yersinia enterocolitica O:3-induced arthritis: triggering bacterial antigens and articular immune response. Rheumatology, 2007;46(4):590-6). For additional information, contact M.S. Di Genaro, National University of San Luis, Laboratory of Microbiology and Immunology, Faculty of Chemistry, Biochemistry and Pharmacy, 5700, San Luis, Argentina. The publisher's contact information for the journal Rheumatology is: Oxford University Press, Great Clarendon St., Oxford OX2 6DP, England. Keywords: Argentina, San Luis, Arthritis Immunology, Arthritis, Immunology, Rheumatology, Yersinia. This article was prepared by Pain & Central Nervous System Week editors from staff and other reports. Copyright 2007, Pain & Central Nervous System Week via NewsRx.com.
|
