Rheumatoid arthritis and enteric bacteria |
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Authors: | Shigehisa Aoki |
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Institution: | (1) Division of Locomotorial Disorders, Institute for Medical Science of Aging, Aichi Medical University, 21 Karimata, Nagakute-cho, 480-1195 Aichi-gun, Aichi-ken, Japan;(2) Present address: Division of Locomotorial Disorders, Institute for Medical Science of Aging, Aichi Medical University, 1206, 5-chome Akaike, 470-0125 Nissin City, Aichi-ken, Japan |
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Abstract: | Factors in the etiopathogenesis of rheumatoid arthritis (RA) include the genetic back-ground, environmental factors and perpetuation
of the inflammatory process. This review focuses on enteric bacteria as initiating or perpetuating factors in the etiopathogenesis
of RA. Based on the hypothesis that entrobacterial antigens that originated from intestinal flora induce rheumatoid inflammation
in the joints, animal models of arthritis due toEnterobacteriaceae, studies on humoral and cellular responses to entrobacterial antigens in RA, etiology of RA involving both genetic and environmental
factors, pathogenesis of rheumatoid inflammation accompanied by joint destruction, and clinical trials with basic therapeutic
considerations are reviewed. The results of immunological studies on RA suggest that some patients with RA are sensitized
to antigens common amongEnterobacteriaceae (bacterial outer membrane proteins of 35 and 38 kDa). A bacterial outer membrane protein of 38 kDa was identified as OmpC
having amino acid homology (NYGVV) with HLA-DR4. This OmpC peptide elicited peripheral blood T cell proliferative responses
in patients with RA. The presentation of this enterobacterial peptide by the RA-associated DR motif to CD4+ T cells could lead to initiation of disease. We now consider that in some patients, RA may be based on autoimmunity from
molecular mimicry by entrobacterial antigens of HLA-DR4. |
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Keywords: | Rheumatoid arthritis enteric bacteria OmpC HLA-DR4 molecular mimicry |
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