Fig. 5. EP receptor signaling and downstream activation of LOXs by PGE₂ lead to lipid mediator class switching and inflammation resolution.

(A) Downstream activity of 15-LO was inhibited using the antagonist PD146176, also causing a significant delay in neutrophil removal from the wound site at 24 hpi. ****P < 0.0001. Data represent three replicates with a minimum of 30 fish per replicate. T test was performed. (B) Varying doses of PD146176 increase neutrophil numbers at the wound site at 24 hpi in a dose-dependent manner. (C) Exogenous PGE₂ is unable to significantly decrease neutrophil numbers in the presence of the 15-LO inhibitor PD146176 at 24 hpi. ***P < 0.001. (D) qPCR expression analysis of alox12 following injury shows a significant increase up to the peak of inflammation. Fold change of expression to the reference gene represents the means ± SEM of four replicate experiments per time point, with a minimum of 50 larvae per replicate, therefore n = 200 individual larvae. P = 0.04, r ² = 0.91.