PGE(2) involvement in experimental Trypanosoma cruzi infection depends
on the lethal capacity of the parasite subpopulation used. Mice acute
ly infected with non-lethal K98 displayed an enhancement in PGE(2) ser
um levels during the acute period, while those infected with lethal T,
cruzi subpopulations (RA or K98-2) showed levels not different from n
ormal mice. The enhancement detected in K98 group could be related bot
h to an increased number of CD8+ T cell number and to enhanced PGE(2)
release per cell by CD8+; values of PGE(2) release by adherent cells w
ere not altered in this group. Treatment with cyclooxygenase inhibitor
s enhanced mortality rates of mice infected with K98, and administrati
on of 16,16-dimethyl PGE(2) (dPGE) reversed this effect. However, mice
infected with RA did not reduce their mortality rates by administrati
on of diverse doses of dPGE. These findings suggest that PGE(2) could
play a role in resistance in mice infected with K98.