Background The study evaluated the relationship between conditioned pathogen clostridium and rheumatoid arthritis (RA) using collagen-induced arthritis (CIA) animal model.

Methods SPF DBA/1 mice were randomly divided into 4 groups (n=6). Enema administration of clostridium which were from RA patients was started on 2 weeks before injection of the II collagen in Mouse and lasted for 5 weeks. Mouse was sacrificed 13 weeks after injection of the II collagen. Serum level of TNF-α, IL-1β and IL-23 were observed, and four-point arthritis indexes were also assessed. Knee joints were assessed according to the histopathology.

Results Arthritis incidence, the number of arthritic limbs per arthritic mouse and the arthritic severity scores were higher in CIA-Clostridium group than the CIA group after the 13 weeks of the immunization, however, the difference was not statistically significant (P>0.05). As compared with the CIA (TNF-α: 239.7±59.9pg/ml, IL-1β: 190.0±55.0pg/ml), the TNF-α: (301.1±19.2pg/ml, P <0.01) and IL-1β (247.2±32.0pg/ml, P<0.05) were significantly increased.

Conclusions Present research suggests that Clostridium may not induce the arthritis directly. Enema administration of Clostridium may have effect on the disease, but the effect was not statistically significant. Clostridium vaccination combining collagen-induced could significantly increase the level of cytokines in peripheral blood of CIA mice, such as TNF-αand IL-1β.

References

1. Vaahtovuo, J., et al., Fecal microbiota in early rheumatoid arthritis. J Rheumatol, 2008. 35(8): p. 1500-5.

2. Brand, D.D., K.A. Latham, and E.F. Rosloniec, Collagen-induced arthritis. Nat Protoc, 2007. 2(5): p. 1269-75.

3. van de Loo, F.A., et al., Role of interleukin-1, tumor necrosis factor alpha, and interleukin-6 in cartilage proteoglycan metabolism and destruction. Effect of in situ blocking in murine antigen- and zymosan-induced arthritis. Arthritis Rheum, 1995. 38(2): p. 164-72.

4. Zhang, F., G. Meng, and W. Strober, Interactions among the transcription factors Runx1, RORgammat and Foxp3 regulate the differentiation of interleukin 17-producing T cells. Nat Immunol, 2008. 9(11): p. 1297-306.

5. Cua, D.J., et al., Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain. Nature, 2003. 421(6924): p. 744-8.

6. Murphy, C.A., et al., Divergent pro- and antiinflammatory roles for IL-23 and IL-12 in joint autoimmune inflammation. J Exp Med, 2003. 198(12): p. 1951-7.

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.1094