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首页> 外文期刊>Proceedings of the Society for Experimental Biology and Medicine >Exposure of macrophages to an enzymatically inactive macrophage mannose receptor ligand augments killing of Candida albicans
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Exposure of macrophages to an enzymatically inactive macrophage mannose receptor ligand augments killing of Candida albicans

机译:巨噬细胞暴露于无酶活性的巨噬细胞甘露糖受体配体会增加白色念珠菌的杀灭

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摘要

Macrophages (M phi) are involved in host defenses against opportunistic pathogens. Previous studies by the present investigators indicate that M phi exposed to enzymatically active myeloperoxidase (MPO), exhibited both increased phagocytosis and killing of Candida albicans. The purpose of this study was to determine if enzymatically inactive M phi-mannose receptor (MMR) ligands could function similarly. Resident murine peritoneal M phi were exposed to the MMR ligands, mannosylated bovine serum albumin (mBSA), and enzymatically inactive myeloperoxidase (iMPO), followed by exposure to opsonized C. albicans. Both mBSA and iMPO induced a slight increase in the number of phagocytizing cells; however, candidacidal activity was significantly higher in treated cultures compared to controls (P less than or equal to 0.001). The production of reactive oxygen Intermediates (ROI) was detected using chemiluminescence. After employment of ROI scavengers, a decrease in candidacidal activity was observed. The data suggest that MMR-ligand interaction alone is sufficient to significantly enhance the candidacidal activity of M phi via ROI, and that iMPO which is released at a site of inflammation induces M phi-mediated killing of microorganisms. These findings indicate a previously unrecognized role of iMPO. [References: 37]
机译:巨噬细胞(M phi)参与针对机会性病原体的宿主防御。本研究人员先前的研究表明,暴露于具有酶活性的髓过氧化物酶(MPO)的M phi表现出增加的吞噬作用和杀死白色念珠菌。这项研究的目的是确定无酶活性的M phi-甘露糖受体(MMR)配体是否可以发挥相似的功能。将居民鼠腹膜M phi暴露于MMR配体,甘露糖基化的牛血清白蛋白(mBSA)和酶促失活的髓过氧化物酶(iMPO),然后暴露于调理的白色念珠菌。 mBSA和iMPO均可诱导吞噬细胞数量的轻微增加;然而,与对照相比,处理过的培养物中的候选酸活性明显更高(P小于或等于0.001)。使用化学发光检测活性氧中间体(ROI)的产生。在使用了ROI清除剂后,观察到了候选酸活动的减少。数据表明,单独的MMR-配体相互作用足以通过ROI显着增强M phi的候选酸活性,并且在炎症部位释放的iMPO诱导M phi介导的微生物杀伤。这些发现表明,iMPO的作用以前未被认识。 [参考:37]

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