During resolution of acute inflammation, the switch from pro-inflammatory to pro-resolving lipid mediators is characterized by:

• A Increased prostaglandin E2 production driving continued vasodilation
• B Upregulation of NF-κB in macrophages producing more TNF-α to amplify the response
• C Conversion of LTB4 to LTC4 shifting the effector profile from neutrophilic to eosinophilic
• D Neutrophil-derived 15-epi-lipoxin A4 (aspirin-triggered lipoxin) and macrophage-derived resolvin D1 inhibiting further neutrophil recruitment and promoting efferocytosis ✓

Explanation

Resolution of acute inflammation is an active process involving biosynthesis of specialized pro-resolving mediators (SPMs). Aspirin-acetylated COX-2 produces 15-epi-lipoxin A4; neutrophil-derived lipoxins and macrophage-derived resolvins (derived from EPA and DHA via 5-LOX/15-LOX) act on distinct receptors to stop neutrophil recruitment, promote neutrophil apoptosis, enhance macrophage efferocytosis of apoptotic neutrophils, and reduce inflammatory cytokine release. This is the physiological 'off-switch' for acute inflammation.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.