{"title":"Infection Protection During Inflammation","authors":"","doi":"10.1126/scisignal.1392002tw236","DOIUrl":null,"url":null,"abstract":"During microbial infection, neutrophils generate microbicidal agents through the release of myeloperoxidase (MPO). Eiserich et al. report that MPO's actions during inflammation extend beyond generating antimicrobial oxidizing species. MPO permeates the mammalian vasculature and alters blood vessel function during acute inflammation by catabolizing nitric oxide (NO). NO is an endothelial-derived blood vessel relaxant that is produced in response to endotoxin. By reducing NO availability, MPO impairs vascular changes produced by infection. This finding may explain the increased susceptibility of humans deficient in MPO to infection. J. P. Eiserich, S. Baldus, M.-L. Brennan, W. Ma, C. Zhang, A. Tousson, L. Castro, A. J. Lusis, W. M. Nauseef, C. R. White, B. A. Freeman, Myeloperoxidase, a leukocyte-derived vascular NO oxidase. Science 296, 2391-2394 (2002). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"34 1","pages":"TW236 - tw236"},"PeriodicalIF":0.0000,"publicationDate":"2002-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Science's STKE","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1126/scisignal.1392002tw236","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
During microbial infection, neutrophils generate microbicidal agents through the release of myeloperoxidase (MPO). Eiserich et al. report that MPO's actions during inflammation extend beyond generating antimicrobial oxidizing species. MPO permeates the mammalian vasculature and alters blood vessel function during acute inflammation by catabolizing nitric oxide (NO). NO is an endothelial-derived blood vessel relaxant that is produced in response to endotoxin. By reducing NO availability, MPO impairs vascular changes produced by infection. This finding may explain the increased susceptibility of humans deficient in MPO to infection. J. P. Eiserich, S. Baldus, M.-L. Brennan, W. Ma, C. Zhang, A. Tousson, L. Castro, A. J. Lusis, W. M. Nauseef, C. R. White, B. A. Freeman, Myeloperoxidase, a leukocyte-derived vascular NO oxidase. Science 296, 2391-2394 (2002). [Abstract] [Full Text]
在微生物感染期间，中性粒细胞通过释放髓过氧化物酶(MPO)产生杀微生物剂。Eiserich等人报道，MPO在炎症中的作用超出了产生抗微生物氧化物质的范围。MPO通过分解一氧化氮(NO)，渗透到哺乳动物的血管中，并在急性炎症期间改变血管功能。一氧化氮是一种内皮来源的血管松弛剂，是对内毒素的反应。通过降低NO的可用性，MPO损害了感染引起的血管变化。这一发现可以解释MPO缺乏的人对感染的易感性增加。J. P.艾塞里奇，S.鲍德斯，M.-L。Brennan, W. Ma, C. Zhang, a . Tousson, L. Castro, a . J. Lusis, W. M. Nauseef, C. R. White, B. a . Freeman，髓过氧化物酶，一种白细胞来源的血管NO氧化酶。科学296,2391-2394(2002)。【摘要】【全文】
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