Role of nitric oxide in the defenses of Crassostrea virginica to experimental infection with the protozoan parasite Perkinsus marinus.

We investigated the role of nitric oxide (NO) in the responses of the Eastern oyster, Crassostrea virginica, to the protozoan parasite Perkinsus marinus, causative agent of Dermo disease. P. marinus induced a slight but significant increase in NO production by oyster hemocytes in vitro, comparable to the increase induced by the immune stimulants phorbol myristrate acetate (PMA) and lipopolysaccharide (LPS). P. marinus also activated the NO response in oysters in vivo, as shown by induction of a protein reacting with a universal NO synthase (NOS) antibody in hemocytes and the presence of high levels of nitrite in plasma. Treatment of experimentally infected oysters with the NOS inhibitor, Nomega-nitro-L-arginine methyl ester (L-NAME) resulted in a transient decrease in NO levels in oyster plasma and a significant increase in the number of parasites at early time points after infection. The NO donor, S-nitroso-N-acetyl-penicillamine (SNAP) caused a significant inhibition in the proliferation of P. marinus cultured cells after 24 h of incubation. These results indicate that NO has a role in decreasing parasite loads at early time points after infection.