ISPO

Prevention of adjuvant arthritis and pristane induced arthritis in lewis rats by incomplete Freund adjuvant (IFA) or complete Freunds adjuvant (CFA)

OK Kohashi, MD, PhD, MA Hossain, CL Zheng, L Zhang, MD, PhD

Saga Medical School, Saga, Saga Japan

Aim: Adjuvant immunotherapy is beneficial in various autoimmne diseases. Adjuvant arthritis (AA) and pristane induced arthritis (PIA) were selected to evaluate the efficacy of adjuvant immunotherapy and to elucidate the pathogenesis of these arthritis models. Methods: Lewis rats were intradermally injected with CFA for induction of AA and with pristane for PIA. IFA was intradermally injected 3-4 weeks before CFA immunization. CFA was intradermally injected before onset of PIA after pristane injection. For therapeutical use, CFA were intradermally injected in the rats with severe PIA. Inguinal lymph node cells (LNCs) were isolated from the individual rats by different immunization schedules and the mRNA expression of the cytokines from the LNCs was determined by RT-PCR. Result: IFA completely prevented the development of AA. CFA prevented not only the development of PIA but also the progression of the established PIA. LNCs of AA developing rats showed the increased mRNA expression of IFN-gamma, IL-2 and TNF-alpha, whereas LNCs of AA prevented rats by IFA showed the increased expression of IL-4 and IFN-gamma but no IL-2 and TNF-alpha. LNCs of PIA developing rats showed the increased expression of IFN-gamma, IL-2 and TNF-alpha, whereas LNCs of PIA prevented or suppressed rats by CFA showed the increased expression of IFN-gamma and TNF-alpha, positive expression of IL-4 and no IL-2. Conclusion: IFA or CFA prevented AA or PIA, respectively. CFA also ameliorated the ongoing PIA. Th1 cytokines or Th2 over Th1 cytokines expression plays an important regulatory role in these disease development or prevention.

KEY WORDS: cytokines, Rats, Th1/Th2 balance.

For more information, contact kohashi@post.saga-med.ac.jp

Paper presented at the International Symposium on Predictive Oncology and Intervention Strategies; Paris, France; February 9 - 12, 2002; in the section on Autoimmunity.

http://www.cancerprev.org/Journal/Issues/26/101/1292/4266