Neutrophil-platelet lipoxins limit tissue damage

This proposed hypothesis asks how inflamed tissue could recover when neutrophil engulfment, removal of these inflammatory immune cells, is blocked. It proposes that suppressing EP2, a receptor for the signalling lipid prostaglandin E2, leaves a neutrophil precursor available to platelets, clot-forming blood components. Platelet-specific 12-lipoxygenase, an enzyme, would convert that precursor into lipoxins, signalling lipids proposed to limit tissue damage. The decisive test would trace the precursor, then inactivate the enzyme. Loss of labelled lipoxins and recovery, followed by restoration with the corresponding product, would support this route. Preserved recovery would keep rival mechanisms in play.