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10.1038/srep33192

http://scihub22266oqcxt.onion/10.1038/srep33192
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C5020415!5020415!27619816
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suck abstract from ncbi


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pmid27619816      Sci+Rep 2016 ; 6 (ä): ä
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  • Involvement of Histamine and RhoA/ROCK in Penicillin Immediate Hypersensitivity Reactions #MMPMID27619816
  • Han J; Yi Y; Li C; Zhang Y; Wang L; Zhao Y; Pan C; Liang A
  • Sci Rep 2016[]; 6 (ä): ä PMID27619816show ga
  • The mechanism of penicillin immediate hypersensitivity reactions has not been completely elucidated. These reactions are generally considered to be mediated by IgE, but penicillin-specific IgE could not be detected in most cases. This study demonstrated that penicillin was able to cause vascular hyperpermeability in a mouse model mimicking clinical symptoms of penicillin immediate hypersensitivity reactions. The first exposure to penicillin also induced immediate edema and exudative reactions in ears and lungs of mice in a dose-dependent manner. Vasodilation was noted in microvessels in ears. These reactions were unlikely to be immune-mediated reactions, because no penicillin-specific IgE was produced. Furthermore, penicillin treatment directly elicited rapid histamine release. Penicillin also led to F-actin reorganization in human umbilical vein endothelial cells and increased the permeability of the endothelial monolayer. Activation of the RhoA/ROCK signaling pathway was observed in ears and lungs of mice and in endothelial cells after treatment with penicillin. Both an anti-histamine agent and a ROCK inhibitor attenuated penicillin immediate hypersensitivity reactions in mice. This study presents a novel mechanism of penicillin immediate hypersensitivity reactions and suggests a potential preventive approach against these reactions.
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