We analysed the production of nitric oxide (NO) intermediates by cells
from BALB/c mice infected with either virulent (Tulahuen or RA) or av
irulent (CA-1) strains of Trypanosoma cruzi. Peritoneal or spleen cell
s from mice infected with T. cruzi released NO when incubated without
further stimuli. Cells from mice during the acute stage of infection a
ccumulated higher levels of inducible NO synthase mRNA and produced bo
th, before and after lypopoly-saccharide stimulation, higher amounts o
f No than cells from mice chronically infected with T. cruzi. NO synth
esis showed similar kinetics in connection with all three strains of T
. cruzi, but cells from mice inbred with the Tulahuen or RA strains re
leased higher levels of IFN-gamma, an activator of the NO pathways, th
an cells from mice infected with the CA-1 strain. In vivo administrati
on of L-Ng-monomethyl-L-arginine (L-NMMA), a competitive inhibitor of
No synthase, increased the susceptibility of mice to T. cruzi. We conc
lude that infection with T. cruzi induces NO production, and suggest t
hat NO plays a role in the resistance against the parasite.