{'fraction_non_alphanumeric': 0.023234200743494422, 'fraction_numerical': 0.0018587360594795538, 'mean_word_length': 6.531468531468532, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Regulation of vascular permeability in anaphylaxis

Anaphylaxis is a life‐threatening type I allergic reaction. Antigen–antibody complexes induce mast cells, basophils and neutrophils to release large amounts of histamine and/or PAF. These mediators induce hypotension and vascular hyper‐permeability and subsequent anaphylaxis dependent on the endothelial production of NO. Here, we have summarized previous studies reporting the mechanisms underlying the functional changes within the vasculature, specifically focusing on vascular permeability triggered by histamine or PAF. In addition to these pro‐inflammatory factors, PGD2 is abundantly released in anaphylaxis, mainly from mast cells. We recently demonstrated that mast cell‐derived PGD2 attenuates anaphylactic responses by inhibiting vascular hyper‐permeability in mouse models. Our findings suggest that pro‐ and anti‐inflammatory factors concurrently regulate vascular permeability in anaphylaxis. In this mini‐review, we discuss the multifactorial mechanisms underlying vascular hyper‐permeability in anaphylaxis.