The resolution phase of acute inflammation involves a class of lipid mediators collectively termed 'specialized pro-resolving mediators' (SPMs). Which statement accurately describes their mechanism?

• A They inhibit COX-2 thereby preventing prostaglandin synthesis from the same arachidonate pool
• B They are glucocorticoid-induced lipocortins that block phospholipase A2 activity non-specifically
• C Lipoxins, resolvins, protectins, and maresins act on specific receptors to inhibit neutrophil recruitment, promote macrophage efferocytosis, and downregulate NF-kB ✓
• D SPMs are leukotriene receptor antagonists that block LTB4-mediated neutrophil chemotaxis

Explanation

Specialized pro-resolving mediators include lipoxins (derived from arachidonic acid via lipoxygenase), resolvins (from EPA/DHA), protectins (from DHA), and maresins (from DHA in macrophages). Unlike anti-inflammatory agents that simply suppress inflammation, SPMs actively promote resolution by: (1) stopping neutrophil recruitment, (2) stimulating macrophage phagocytosis of apoptotic neutrophils (efferocytosis), (3) promoting tissue repair, and (4) downregulating NF-kB signaling. Lipoxin A4 acts via ALXR/FPR2 receptors. Glucocorticoids induce annexins (formerly lipocortins), which inhibit phospholipase A2 — a different mechanism.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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