Enhanced biosynthesis of prostaglandin (PG)D-2 and subsequent formation of 15-deoxy-Delta(12,14)-PGJ(2) has been suggested to contribute to resolution of inflammation. The primary aim of the present study in mouse heart was, therefore, to determine at the transcriptional level if there is sequential induction of PGE and PGD synthases (S) during inflammation. Expression of interleukin (IL)-1 beta in heart was enhanced 4 h after systemic inflammation and declined thereafter within 3-5 days to basal levels. In contrast to cyclooxygenase-2 and membrane-bound (m)-PGES-1, which both peaked 4 It after endotoxin administration, hematopoietic (H)-PGDS expression was enhanced only >= 48 h after endotoxin. The expression of lipocalin-type (L)-PGDS was not significantly influenced. mRNA encoding the putative target of 15-deoxy-Delta(12,14)-PGJ(2), peroxisome proliferator-activated receptor gamma, was enhanced between 4 and 24 h after induction of inflammation. Treatment of mice with acetylsalicylic acid or indomethacin at doses effective to cause near-complete inhibition of PGE(2) and PGD(2) biosynthesis in heart ex vivo resulted in enhanced expression of IL-1 beta 24 h after endotoxin administration. These results provide additional support for the hypothesis of a shift towards PGD, biosynthesis during resolution of inflammation. (C) 2005 Elsevier Inc. All rights reserved.