That production of plasminogen activator by inflammatory macrophages can be inhibited by immunomodulators of bacterial origin, especially lipopolysaccharide (LPS), was previously shown. In these experiments, the contribution of prostaglandins to this control was investigated using 2 prostagladin synthetase blockers, indomethacin and diclofenac. These drugs do not modify per se the production of plasminogen activator in mouse macrophages elicited with killed streptococci, but they can partially prevent the inhibitory effect of Salmonella enteritidis LPS. Since restoration was not complete when plasminogen activator production was strongly inhibited, the immunomodulator probably acts through a mechanism involving more > 1 pathway, only 1 of which would be mediated by prostaglandins.