Our previous finding, that germ‐free F344 rats develop severe adjuvant‐induced arthritis, whereas specific pathogen–free rats develop mild disease, prompted us to investigate the role of bacterial flora in promoting the development of this disease. Germ‐free rats given Escherichia coli experienced disease suppression. Germ‐free rats treated with 3 strains of Lactobacillus experienced an enhancement of the disease, although it was not significant. Germ‐free rats treated with a combination of E coli and lactobacilli had disease suppression similar to that of E coli monoassociated rats. Thus, these findings suggest that E coli may play a dominant role in modulating the development of the disease in this particular strain of F344 rats, possibly through its lipopolysaccharide (as evidenced by positive results on limulus tests). These findings also suggest that microflora play an important role in modifying the development of joint disease.

Germfree (GF) F344 rats developed severe adjuvant-induced arthritis with a 100% incidence after a single intradermal injection of heat-killed Mycobacter i u m bovis (BCG). Specific pathogene-free (SPF) rats developed less severe arthritis with a lower incidence. The rats colonized with Escherichia coli or Bacteroides developed mild disease comparable to that in SPF rats. The rats colonized with Bifidobacteri u m, Propionibacterium acnes, Lactobacillus casei, L. fermentum, L. murini, and L. acidophil u s developed more severe disease than that in GF rats. Furthermore, the rats colonized with a mixture of E. coli and the above lactobacilli developed very mild disease similar to that in SPF rats. These results suggest that (1) gram-negative bacteria, such as E. coli and Bacteroides, may suppress the disease, possibly through their lipopolysaccharides, and may be responsible for the lower susceptibility of SPF rats ; (2) gram-positive bacteria, such as Bifidobacterium, P. acnes, and lactobacilli, may enhance the disease, possibly through their peptidoglycans; and (3) E. coli may play a dominant role in modulating the development of adjuvant-induced arthritis.

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