Mechanisms underlying vascular hyperpermeability in allergic inflammation

Abstract

In allergic inflammation (type I hypersensitivity), the antigen-antibody reaction triggers mast cell degranulation. Inflammatory mediators released by activated mast cells induce vascular hyperpermeability, leading to pronounced inflammation. Understanding these mechanisms is essential for developing novel therapeutic strategies. Vascular permeability is primarily regulated by blood flow and endothelial barrier function. In this review, we summarize how mediators such as histamine, platelet-activating factor, bradykinin, prostaglandin D₂, and tumor necrosis factor-α modulate vascular permeability, with a focus on their effects on blood flow and endothelial barrier function in allergic inflammation.