sm-10906 and Pleurisy

Prostaglandins E1, prostaglandin E2, 3-oxa-methano-prostaglandin I1 (SM-10906), a stable prostaglandin I2 analog, and dibutyryl cyclic AMP suppressed the production of tumor necrosis factor and interleukin-1 in lipopolysaccharide-stimulated rat pleural resident monocytic cells, whereas they enhanced the production of interleukin-6 and cytokine-induced neutrophil chemoattractant (CINC), a rat interleukin-8-like chemokine, in these cells. SM-10906 also inhibited the in vivo production of tumor necrosis factor and interleukin-1 in pleural exudates, when injected into the rat pleural cavity concomitantly with carrageenin. The cyclic AMP (cAMP) level in the lipopolysaccharide-stimulated resident cells was increased when the cells were incubated in the presence of prostaglandin E1, prostaglandin E2 or SM-10906. Prostaglandin I2 showed only slight effects. The addition of pentoxifylline, a phosphodiesterase inhibitor, to the incubation mixture increased the cAMP level and also enhanced the effect of prostaglandins, indicating that these regulating actions of prostaglandins may be exerted partly through a mechanism involving an increased intracellular cAMP level.

Topics: Alprostadil; Animals; Bucladesine; Carrageenan; Cell Line; Chemokine CXCL1; Chemokines, CXC; Chemotactic Factors; Cyclic AMP; Cytokines; Dinoprostone; Epoprostenol; Excipients; Female; Growth Substances; Intercellular Signaling Peptides and Proteins; Leukocytes; Male; Mice; Mice, Inbred C3H; Oxytocics; Pentoxifylline; Phosphodiesterase Inhibitors; Platelet Aggregation Inhibitors; Pleurisy; Rats; Rats, Sprague-Dawley