MACROPHAGE ACTIVITY, IL-6 LEVELS, ANTIBODY-RESPONSE AND HEART HISTOLOGY IN RATS UNDERGOING AN ATTENUATED TRYPANOSOMA-CRUZI ACUTE INFECTION UPON TREATMENT WITH RECOMBINANT INTERFERON-GAMMA

Earlier experiments in Trypanosoma cruzi-infected rats showed that rec ombinant rat (Rr) interferon (IFN)-gamma given shortly after infection ameliorated acute disease without modifying the serum titers of endog enously synthesized IFN-gamma and tumor necrosis factor. To gain some insight into the processes underlying this protective effect, 21-day o ld 'I' rats that were infected with T., cruzi and the following day st arted with a 20-day cycle of RrIFN-gamma injections (20 000 IU/rat/day ) were investigated for the in vitro replication of T. cruzi and nitri c oxide (NO) production by peritoneal macrophages (day 7 post-infectio n, pi), antibodies with lyric activity against T. cruzi (days 7, 20, a nd 28 pi), and serum levels of biologically active interleukin (IL)6 ( days 15 and 30 pi). Therapy with RrIFN-gamma rendered cultured periton eal macrophages less permissive to infection with T. cruzi. Such an ef fect was not accompanied by higher amounts of NO in macrophage culture d supernatants, compared with those from T. cruzi-infected rats receiv ing no RrIFN-gamma, which appeared not to be protected from in vitro i nfection. Acutely 7. cruzi-infected rats had significant amounts of IL -6 in their sera - this not being the case in infected rats given RrIF N-gamma, whose levels appeared decreased as in control rats. The prese nce of complement-mediated anti-T. cruzi lytic antibodies was not modi fied by RrIFN-gamma. Likewise, heart histology at day 7 pi revealed th at treatment with RrIFN-gamma made no differences as to the amount of acute inflammation, but tended to reduce the myocardial parasite load.