Nitric oxide in parasitic infections

Nitric oxide (NO) is implicated as an integral component of the host armament against invading parasites. Strongest evidence has come from laboratory models of protozoan infections. During malaria, toxoplasmosis and leishmaniasis, to name just a few, the preferential production of pro-inflammatory cytokines predisposes to the increased synthesis of NO, which mediates host protection through either direct parasite killing or by limiting parasite growth. More recently, evidence has been put forward for a beneficial role of NO during helminthic infections. In the case of Schistosomiasis mansoni, for example, NO plays a role in regulation of egg-induced inflammation, preventing hepatocyte death and widespread tissue damage. In spite of these findings, rather than being the ultimate panacea, NO production requires tight control to limit cytotoxic damage to the host's own cells. Unregulated production may lead to a variety of damaging effects including alterations to normal neurological functions during cerebral malaria and intestinal pathology during trichinosis. In this review, I will summarize the role of NO during a number of parasitic infections, drawing on specific examples of disease caused by protozoan and metazoan parasites.