Question:
Increased vascular permeability in acute inflammation is mainly due to which mediator?
Increased vascular permeability in acute inflammation is mainly due to which mediator?
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Which preformed mast-cell mediator causes the immediate transient venular leak?
Updated On: Jun 24, 2026
- Histamine
- IL-2
- TGF-beta
- FGF
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The Correct Option is A
Solution and Explanation
Step 1: A hallmark of acute inflammation is increased vascular permeability, which lets protein-rich fluid leave the vessels and form exudate. The commonest mechanism is the formation of endothelial gaps in venules, also called the immediate transient response.
Step 2: This gap formation is driven by vasoactive mediators that cause endothelial cell contraction. Histamine is the prototype and most important immediate mediator, along with bradykinin, leukotrienes and substance P. Histamine is released rapidly from mast cells, basophils and platelets, making it the first responder.
Step 3: The distractors do not fit. IL-2 is a T-cell growth cytokine of adaptive immunity. TGF-beta is an anti-inflammatory and fibrogenic cytokine involved in repair, not permeability. FGF is a growth factor active in angiogenesis and healing. None of these mediate the immediate permeability change.
Step 4: Hence histamine is the mediator responsible for increased permeability in acute inflammation.
Step 2: This gap formation is driven by vasoactive mediators that cause endothelial cell contraction. Histamine is the prototype and most important immediate mediator, along with bradykinin, leukotrienes and substance P. Histamine is released rapidly from mast cells, basophils and platelets, making it the first responder.
Step 3: The distractors do not fit. IL-2 is a T-cell growth cytokine of adaptive immunity. TGF-beta is an anti-inflammatory and fibrogenic cytokine involved in repair, not permeability. FGF is a growth factor active in angiogenesis and healing. None of these mediate the immediate permeability change.
Step 4: Hence histamine is the mediator responsible for increased permeability in acute inflammation.
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