Arachidonic acid-derived lipoxins differ from prostaglandins and leukotrienes in that they primarily function to:
- A Amplify neutrophil recruitment and vascular permeability
- B Cause bronchoconstriction and increase vascular permeability
- C Act as pro-resolving mediators inhibiting neutrophil trafficking and promoting macrophage phagocytosis of apoptotic cells ✓
- D Activate platelet aggregation and thromboxane synthesis
Explanation
Lipoxins are specialised pro-resolving mediators (SPMs) derived from arachidonic acid via 15-LOX and 5-LOX pathways. They act as 'stop signals' for inflammation: inhibiting neutrophil recruitment, promoting non-phagocytic clearance of apoptotic cells (efferocytosis) by macrophages, and stimulating pro-resolving mediator production. This distinguishes them fundamentally from prostaglandins and leukotrienes, which amplify vascular permeability and leukocyte recruitment. Resolvins and protectins (from EPA/DHA) act similarly.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.