SKG mice are a recently established experimental model for
rheumatoid arthritis (RA). Although they spontaneously develop chronic autoimmune
arthritis under conventional conditions, SKG mice failed to develop chronic
arthritis in a strictly controlled specific pathogen-free (SPF) environment.
Beta-glucan (BG) from Laminaria digitata,
laminarin (
LAM), induced
arthritis under SPF conditions, thus BG would be a pathogenic factor for
arthritis in SKG mice. Therefore, we prepared BG from Candida albicans, a pathogenic fungus and investigated whether BG from C. albicans induced
arthritis in SKG mice under SPF conditions. SKG mice were injected intraperitoneally with particulate BG (oxidative-Candida albicans (OX-CA)), soluble BG (Candida soluble
beta-glucan (CSBG)) from C. albicans and
LAM as a positive control. In addition,
schizophyllan (SPG) from Schizophyllum commune or Mycobacterium whole cells were injected into SKG mice to induce
arthritis. Mice injected with OX-CA, CSBG and SPG had more severe
arthritis than with
LAM, and whole Mycobacterium cells.
IL-6 concentration in sera from SKG mice injected with OX-CA or CSBG was high, whereas not detected in sera from mice treated with
LAM. In histological analysis, infiltration of inflammatory cells was observed in SKG mice injected with BG. These results suggest that
fungal infection may be
a factor to induce and exacerbate
autoimmune diseases such as RA.