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. 2022 Jan 25;180:236–243. doi: 10.1016/j.freeradbiomed.2022.01.021

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Fig. 4 — Cellular and oxylipin interplay during the evolution of an inflammatory process. Phase 1 and Phase 2: rapid neutrophil and delayed monocyte extravasation in response to cytokines produced by activated immune tissue-resident cells. Pro-inflammatory oxylipins are produced mainly by neutrophils, M1-macrophages, activated endothelial cells and platelets. Phase 3: neutrophil apoptotic bodies and prostaglandins promote the macrophage shift towards a resolution-phase function. Phase 4: inflammation resolution is promoted by increasing production of the specialized pro-resolving mediators. PGE₂: prostaglandin E₂; PGD₂: prostaglandin D₂; PGI₂: prostacyclin I₂; TX-A₂: thromboxane A₂; LTA₄: leukotriene A₄; LTB₄: leukotriene B₄; Cys-LT: cysteine-leukotrienes; EETs: epoxyeicosatrienoic acids; COX-1: cyclooxygenase-1; COX-2: cyclooxygenase-1; 5-LOX: 5-lipoxygenase; 15-LOX: 15-lipoxygenase.