Influence of a cytomegalovirus infection on functions and arachidonic acid metabolism of rat peritoneal macrophages.

An intraperitoneal (rat) cytomegalovirus (RCMV) infection in the rat caused an influx of mononuclear cells, which have been altered in functions and arachidonic acid (AA) metabolism. Phagocytosis has been increased considerably 3 days postinfection (p.i.), whereas the release of prostacyclin, thromboxane A2, 12-hydroxyheptadecatrienoic acid (HHT), 5-hydroxyeicosatetraenoic acid (5-HETE), and leukotriene B4 (LTB4) was inhibited for more than 80%. The release of superoxide anions and the chemiluminescence response (CL) upon opsonized zymosan stimulation did not differ from those observed in resident peritoneal macrophages. Additionally, the levels of cyclic nucleotides (cAMP and cGMP) were low in both resident and influx macrophages (day 3 p.i.). In contrast, peritoneal macrophages harvested on day 10 p.i. still showed a high level of phagocytosis. However, the intracellular level of cyclic AMP had decreased fivefold, whereas CL response and superoxide anion release were inhibited significantly. Moreover, the production of prostacyclin, LTB4, and 5-HETE was still suppressed in contrast to thromboxane synthesis, which has selectively been restored in these macrophages. A direct regulatory role of AA metabolites in changes in macrophage functions that were due to a RCMV infection could not be demonstrated.