Complement fragment C5a is one of the most potent pro-inflammatory mediators. In addition to being a chemoattractant, C5a exerts which direct effect on vascular endothelium during acute inflammation?

• A Stimulates P-selectin expression on endothelial cells and mast cell degranulation, causing increased vascular permeability ✓
• B Upregulates ICAM-1 only on venule endothelium through NF-κB pathway
• C Directly activates endothelial eNOS causing vasodilation
• D Promotes VEGF secretion causing long-term angiogenesis

Explanation

C5a acts directly on mast cells and basophils to stimulate degranulation and histamine release, which in turn acts on venular endothelium to cause P-selectin surface expression and endothelial contraction — both increasing vascular permeability. C5a also directly upregulates P-selectin on endothelial cells. C5a additionally acts as a potent neutrophil and monocyte chemoattractant, activates neutrophil oxidative burst, and amplifies leukotriene production. Together, C5a links complement activation to the acute vascular and cellular phases of inflammation.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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