Tissue distribution and persistence of arthritogenic and non-arthritogenicEubacterium cell walls

Objective To study the tissue distribution and persistence of arthritogenic and non-a rthritogenic Eubacterium cell walls (CWs), using arthritogenic Eubacterium aerofaciens and non-arthritogenic Eubacterium limosum. Methods Eubacterium aerofaciens ol Eubacterium limosum CW was injected into Lewis r ats intraperitoneally. Inflammatory changes in the synovium and periarticul ar tissues were graded histologically. On days 14 28 and 56 after the injec tion, the presence of CW in the liver; spleen, mesenteric lymph nodes and s ynovium was studied by indirect immunofluorescence. In parallel, CW-derived muramic acid in the liver and spleen was measured by gas chromatography-ma ss spectrometry. In addition, serum TNF-alpha, IL-1 beta and IL-10 concentr ations were determined by ELISA. Results Systemic injection of Eubacterium aerofaciens CW, but not of Eubacterium li mosum CW, resulted in chronic arthritis. Both E. aerofaciens and E. limosum CWs were observed in the liver and spleen at all of the time points studie d. In addition, Eubacterium limosum CW was present in non-arthritic synoviu m on day 14. It was not, however, detected in the synovium or lymph nodes o n days 28 and 56 in clear contrast to the rats injected with E. aerofaciens CW. According to the analysis by gas chromatography-mass spectrometry, non arthritogenic E. limosum CW had accumulated in the liver cells on days 14 a nd 28 after the injection to a greater extent than arthritogenic E. aerofac iens CW, leading to a lesser distribution in the other organs. A weak trend was observed suggesting that the production of TNF-alpha and IL-1 beta, bu t not of IL-10, is stimulated better by arthritogenic CW than by non-arthri togenic CW. Conclusion Our results indicate that non-arthritogenic CWs are handled by the rat's de fence mechanisms in a different way than arthritogenic CWs. The tissue dist ribution and persistence of CWs play a role in arthritogenicity, but additi onal factors must exist to determine why the CWs of certain bacteria are ar thritogenic and those of others are not.