Treatment of the human lung fibroblast cell line, WI-38, with interleukin-1 alpha (IL-1 alpha) results in a large increase in the production of cytosolic phospholipase A2 (cPLA2) and prostaglandin E2 (PGE2). The IL-1-induced accumulation of cPLA2 is closely correlated with increased PGE2 release. In contrast to cPLA2, the level of cyclooxygenase remains unchanged following IL-1 alpha treatment. The glucocorticoid, dexamethasone, blocks the IL-1 alpha-mediated increases in both cPLA2 and PGE2 without affecting the cyclooxygenase level. Taken together, these data suggest that in these cells, the regulation of prostaglandin production by IL-1 and glucocorticoid can be attributed to the level of cPLA2. These results provide a new mechanism for the effect of IL-1 and glucocorticoids on eicosanoid synthesis and provide additional support for an important role of cPLA2 in the inflammatory response.
No takes yet. Share an insight, caveat, or question.
Lin et al. (1992) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: