Prostaglandin E2 depresses antigen-presenting cell function of peritoneal macrophages

Eicosanoids play a prominent role in trauma. Such mediators of inflammation negatively influence cell-mediated immunity (CMI). There is, however, no information available on the effect of eicosanoids on a critical event in CMI, i.e., antigen-presenting (AP) cell function of macrophages (M luminal diameter), a cellular process responsible for the activation of T and B lymphocytes. The aim of this study, therefore, was to examine the effect of prostaglandin E2 (PGE2) and thromboxane B2 (TXB2) on AP cell function of the peritoneal M luminal diameter. To study this, a T-helper-cell clone, D10.G4.1 was employed. This cell clone proliferates in the presence of Iak (Class II glycoprotein, MAC product) bearing M luminal diameter and specific antigen (conalbumin A) thus directly reflecting the AP capability of the M luminal diameter. Peritoneal M luminal diameter were harvested from B10.BR mice (H2k) and their AP was tested in vitro by incubating varying numbers of M luminal diameter with 2 X 10(4) D10.G4.1 cells/well and conalbumin (400 micrograms/ml) in the presence and absence of different concentrations of PGE2 or TXB2. Cultures were incubated for 72 hr, pulsed with [3H]-thymidine, and harvested. At concentrations of 10, 30, and 100 nM of PGE2, D10.G4.1 proliferations were 38, 35, and 20% of control, respectively (P less than 0.05 compared to control). TXB2 added at the above-mentioned concentrations did not suppress the proliferative response of D10. Thus, PGE2 but not TXB2 has a potent immunosuppressive effect on AP of peritoneal M luminal diameter.