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The Journal of Immunology, Vol 146, Issue 11 3971-3976, Copyright © 1991 by American Association of Immunologists
ARTICLES |
S Mellouk, SJ Green, CA Nacy and SL Hoffman
Malaria Program, Naval Medical Research Institute, Bethesda, MD 20889- 5055.
Primary cultures of BALB/cJ hepatocytes treated with 10(3) U/ml rIFN- gamma consistently inhibited intracellular Plasmodium berghei liver schizont development by 50 to 70%. Monomethyl-L-arginine (NGMMLA), the competitive inhibitor of L-arginine as substrate for production of nitric oxides by hepatocytes, reversed the activity of IFN-gamma on these malaria-infected cells. Reversal of IFN-gamma activity by NGMMLA was dose dependent and was maximal at 0.5 mM NGMMLA. Depletion of L- arginine by addition of arginase to the culture medium blocked the capacity of IFN-gamma to inhibit parasite development in hepatocytes; addition of excess L-arginine to cultures treated with IFN-gamma in the presence of NGMMLA competitively restored IFN-gamma capacity to activate hepatocyte anti-parasite activity. TNF-alpha was neither required for IFN-gamma activity, nor effective at any concentration tested as an inhibitor of schizont development by itself in primary hepatocytes. These data strongly suggest that the action of IFN-gamma on P. berghei-infected hepatocytes is to induce the production of L- arginine-derived nitrogen oxides that are toxic for the intracellular parasite.
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