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We have tested the hypothesis that nitric oxide may be responsible for the immunosuppression reported during malaria infections. We first showed that reactive nitrogen intermediates, which indicate nitric oxide generation, were increased in the plasma of Plasmodium vinckei-infected mice. We next found that Concanavalin A-induced proliferation of spleen cells from these mice was reduced compared with that observed in uninfected animals. The addition of NG-methyl-L-arginine (L-NMMA) for the duration of the cultures restored the malarial proliferative response to normal. We then tested the effect of oral L-NMMA on the proliferative response of P. chabaudi-infected mice to a human red blood cell lysate. The secondary response to this antigen, measured as spleen cell proliferation in vitro ten days after immunization and when there was no discernible parasitaemia, remained normal in L-NMMA-treated P. chabaudi mice, but was decreased in the untreated infected mice. These results suggest a role for nitric oxide in malarial immunosuppression.

Original publication

DOI

10.1111/j.1365-3024.1994.tb00346.x

Type

Journal article

Journal

Parasite immunology

Publication Date

05/1994

Volume

16

Pages

243 - 249

Addresses

John Curtin School of Medical Research, Canberra, Australia.

Keywords

Spleen, Erythrocytes, Cells, Cultured, Animals, Mice, Inbred CBA, Humans, Mice, Plasmodium chabaudi, Malaria, Nitric Oxide, Arginine, omega-N-Methylarginine, Concanavalin A, Lymphocyte Activation, Cell Division, Immune Tolerance, Male