This study investigates the inducible isoforms of cyclooxygenase (COX) and nitric-oxide synthase (NOS) in a murine air pouch model of granulomatous inflammation. The research focuses on the acute, chronic, and resolving stages of inflammation. COX and NOS activities were measured in skin samples and granulomatous tissue. COX-1 and COX-2 proteins were assessed using Western blot. The results show that COX-2 protein levels increase over time, peaking at day 14. iNOS activity increases in the skin during the first 24 hours and then rises further in granulomatous tissue between days 3 and 7, followed by a decrease at day 14 and an increase at day 21. In the acute phase, COX and NOS activities in the skin increase, reinforcing their proinflammatory roles. However, in the chronic and resolving stages, a dissociation of COX and NOS activity occurs, suggesting differential regulation of these enzymes, possibly due to changes in cytokine patterns during the inflammatory response. The study highlights the complex roles of prostanoids and nitric oxide in inflammation, with prostanoids involved in all stages and nitric oxide playing a proinflammatory role in chronic inflammation. The findings suggest that COX-2 and iNOS are induced by various proinflammatory stimuli, including cytokines, and their activities are regulated by factors such as transforming growth factor beta. The study also discusses the potential modulatory effects of NO on COX activity and the complex roles of PGs in both acute and chronic inflammation. The research provides insights into the regulation of COX and NOS in inflammation and their potential therapeutic implications.This study investigates the inducible isoforms of cyclooxygenase (COX) and nitric-oxide synthase (NOS) in a murine air pouch model of granulomatous inflammation. The research focuses on the acute, chronic, and resolving stages of inflammation. COX and NOS activities were measured in skin samples and granulomatous tissue. COX-1 and COX-2 proteins were assessed using Western blot. The results show that COX-2 protein levels increase over time, peaking at day 14. iNOS activity increases in the skin during the first 24 hours and then rises further in granulomatous tissue between days 3 and 7, followed by a decrease at day 14 and an increase at day 21. In the acute phase, COX and NOS activities in the skin increase, reinforcing their proinflammatory roles. However, in the chronic and resolving stages, a dissociation of COX and NOS activity occurs, suggesting differential regulation of these enzymes, possibly due to changes in cytokine patterns during the inflammatory response. The study highlights the complex roles of prostanoids and nitric oxide in inflammation, with prostanoids involved in all stages and nitric oxide playing a proinflammatory role in chronic inflammation. The findings suggest that COX-2 and iNOS are induced by various proinflammatory stimuli, including cytokines, and their activities are regulated by factors such as transforming growth factor beta. The study also discusses the potential modulatory effects of NO on COX activity and the complex roles of PGs in both acute and chronic inflammation. The research provides insights into the regulation of COX and NOS in inflammation and their potential therapeutic implications.