百日咳博德特氏菌可诱导人多形核白细胞的呼吸爆发活性。
Bordetella pertussis induces respiratory burst activity in human polymorphonuclear leukocytes.
作者信息
Steed L L, Akporiaye E T, Friedman R L
机构信息
Department of Microbiology and Immunology, University of Arizona, Tucson 85724.
出版信息
Infect Immun. 1992 May;60(5):2101-5. doi: 10.1128/iai.60.5.2101-2105.1992.
Virulent Bordetella pertussis strains survive intracellularly within human polymorphonuclear leukocytes (PMN), at least in part because of inhibition of phagosome-lysosome fusion (L. L. Steed, M. Setareh, and R. L. Friedman, J. Leukocyte Biol. 50:321-330, 1991). Further investigations were done to determine if B. pertussis also inhibited respiratory burst activity of PMN as an additional mechanism of intracellular survival. Chemiluminescence and flow cytometry assays showed that B. pertussis induced significant levels of hydrogen peroxide production. In contrast, ferricytochrome c reduction showed that B. pertussis suppressed extracellular release of superoxide. PMN intracellular reduction of nitroblue tetrazolium verified that superoxide was indeed produced intracellularly during B. pertussis phagocytosis. Therefore, B. pertussis does not inhibit production of superoxide but inhibits only its release. Thus, while phagosome-lysosome fusion is inhibited by B. pertussis, respiratory burst activity of PMN occurs at normal levels.
强毒力的百日咳博德特氏菌菌株能在人类多形核白细胞（PMN）内存活，至少部分原因是其抑制了吞噬体与溶酶体的融合（L. L. 斯蒂德、M. 塞塔雷和R. L. 弗里德曼，《白细胞生物学杂志》50:321 - 330，1991年）。开展了进一步研究以确定百日咳博德特氏菌是否也抑制PMN的呼吸爆发活性，作为其细胞内存活的一种额外机制。化学发光和流式细胞术检测表明，百日咳博德特氏菌可诱导产生显著水平的过氧化氢。相比之下，高铁细胞色素c还原实验表明，百日咳博德特氏菌可抑制超氧化物的细胞外释放。PMN对硝基蓝四氮唑的细胞内还原作用证实，在百日咳博德特氏菌吞噬过程中，细胞内确实产生了超氧化物。因此，百日咳博德特氏菌并不抑制超氧化物的产生，而仅抑制其释放。所以，虽然百日咳博德特氏菌抑制了吞噬体与溶酶体的融合，但PMN的呼吸爆发活性仍处于正常水平。
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