Rheumatoid arthritis and enteric bacteria

Abstract

Factors in the etiopathogenesis of rheumatoid arthritis (RA) include the genetic background, 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 to Enterobacteriaceae, 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 among Enterobacteriaceae (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.

The effectiveness of Echinacea extract or composite glucosamine, chondroitin and methyl sulfonyl methane supplements on acute and chronic rheumatoid arthritis rat model

“…In the present work, most of these features were estimated. The OMP prepared from the selected strains of human intestinal flora induced acute and chronic arthritis in rat models, this means that the isolates of E. coli , Citrobacter , Enterobacter , Samonella , Pseudomonas , S. aureus and Streptococcus may have arthropathic properties through the identified moderate inflammatory cellular infiltration, oedema with mild synovial cells proliferation, damaged cartilage layer in the paw joint of the OMP arthritis-induced rats which are in line with the previously mentioned characteristics (Bainbridge et al, 2007; Feldmann et al, 1996; FitzGerald and Bresnihan, 1995; Goldenberg and Cohen, 1978; Wen et al, 2010) and support the previous studies about the etiologic role of the used bacterial OMP in RA (Aoki, 1999; Newkirk et al, 2010; Singh et al, 2011).…”

Commensal Flora, is it an Unwelcomed Companion as a Triggering Factor of Autoimmune Pancreatitis?

“…The link has been attributed to either molecular mimicry between pathogen-derived antigens and self antigens or non-specific activation of innate immunity leading to a breakdown in immunological tolerance and the development of self antigen-specific T cell and antibody response (Mills, 2011 ). A common recent theory of the cause of autoimmune diseases is that an infectious agent triggers a cycle of events, which leads to the upregulation of the host immune response to self antigens (Aoki, 1999 ; Tlaskalová-Hogenova et al, 2004 ).…”

Are Dysregulated Inflammatory Responses to Commensal Bacteria Involved in the Pathogenesis of Hepatobiliary-Pancreatic Autoimmune Disease? An Analysis Using Mice Models of Primary Biliary Cirrhosis and Autoimmune Pancreatitis

“…In Guillain-Barré syndrome (GBS), amino acid similarities exist between the gangliosides of the nerve system and the lipopolysaccharides (LPSs) of Campylobacter jejuni , suggesting that sensitization by microbes may be based on autoimmunity from molecular mimicry between bacteria and the targeted system of the host [ 3 , 4 ]. A common recent theory of the cause of autoimmune diseases is that an infectious agent triggers a cycle of events, which leads to the upregulation of the host immune response to self-antigens [ 5 , 6 ].…”