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• W2185555626 startingPage "G544" @default.
• W2185555626 abstract "Toxin A (TxA) of Clostridium difficile induces acute inflammation of the intestine initiated by release of substance P (SP) and activation of the neurokinin-1 receptor. However, the mechanisms that terminate this response are unknown. We determined whether the SP-degrading enzyme neutral endopeptidase (NEP, EC 3.4.24.11) terminates TxA-induced enteritis. We used both genetic deletion and pharmacological inhibition of NEP to test this hypothesis. In wild-type mice, instillation of TxA (0.5-5 microg) into ileal loops for 3 h dose dependently increased ileal fluid secretion, stimulated granulocyte transmigration determined by myeloperoxidase activity, and caused histological damage characterized by depletion of enterocytes, edema, and neutrophil accumulation. Deletion of NEP reduced the threshold secretory and inflammatory dose of TxA and exacerbated the inflammatory responses by more than twofold. This exacerbated inflammation was prevented by pretreatment with recombinant NEP. Conversely, pretreatment of wild-type mice with the NEP inhibitor phosphoramidon exacerbated enteritis. Thus NEP terminates enteritis induced by C. difficile TxA, underlying the importance of SP degradation in limiting neurogenic inflammation." @default.
• W2185555626 created "2016-06-24" @default.
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• W2185555626 date "2001-08-01" @default.
• W2185555626 modified "2023-10-17" @default.
• W2185555626 title "Deletion of neutral endopeptidase exacerbates intestinal inflammation induced by<i>Clostridium difficile</i>toxin A" @default.
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• W2185555626 doi "https://doi.org/10.1152/ajpgi.2001.281.2.g544" @default.
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