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Guinea pig alveolar macrophages probably kill M. tuberculosis H37Rv and H37Ra in vivo by producing hydrogen peroxide.

作者信息

Jackett P S, Andrew P W, Aber V R, Lowrie D B

出版信息

Adv Exp Med Biol. 1983;162:99-104. doi: 10.1007/978-1-4684-4481-0_10.

DOI:10.1007/978-1-4684-4481-0_10
PMID:6408908
Abstract
摘要

相似文献

1
Guinea pig alveolar macrophages probably kill M. tuberculosis H37Rv and H37Ra in vivo by producing hydrogen peroxide.
Adv Exp Med Biol. 1983;162:99-104. doi: 10.1007/978-1-4684-4481-0_10.
2
Guinea-pig alveolar macrophage killing of Mycobacterium tuberculosis, in vitro, does not require hydrogen peroxide or hydroxyl radical.
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Guinea-pig alveolar macrophages kill Mycobacterium tuberculosis in vitro, but killing is independent of susceptibility to hydrogen peroxide or triggering of the respiratory burst.
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Release of superoxide and hydrogen peroxide from guinea-pig alveolar macrophages during phagocytosis of Mycobacterium bovis BCG.
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Hydrogen peroxide and superoxide release by alveolar macrophages from normal and BCG-vaccinated guinea-pigs after intravenous challenge with Mycobacterium tuberculosis.结核分枝杆菌静脉内攻击后，正常豚鼠和卡介苗接种豚鼠的肺泡巨噬细胞释放过氧化氢和超氧化物的情况。
Br J Exp Pathol. 1981 Aug;62(4):419-28.
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The viable Mycobacterium tuberculosis H37Ra strain induces a stronger mouse macrophage response compared to the heat-inactivated H37Rv strain.活的结核分枝杆菌 H37Ra 株比热失活的 H37Rv 株诱导更强的小鼠巨噬细胞反应。
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Guinea pig neutrophils infected with Mycobacterium tuberculosis produce cytokines which activate alveolar macrophages in noncontact cultures.感染结核分枝杆菌的豚鼠中性粒细胞会产生细胞因子，这些细胞因子在非接触培养中激活肺泡巨噬细胞。
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Differences in mannose receptor-mediated uptake of lipoarabinomannan from virulent and attenuated strains of Mycobacterium tuberculosis by human macrophages.人类巨噬细胞对来自结核分枝杆菌强毒株和减毒株的脂阿拉伯甘露聚糖的甘露糖受体介导摄取的差异。
J Immunol. 1996 Nov 15;157(10):4568-75.
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Macrophage phagocytosis of virulent but not attenuated strains of Mycobacterium tuberculosis is mediated by mannose receptors in addition to complement receptors.除补体受体外，甘露糖受体介导巨噬细胞对结核分枝杆菌强毒株而非减毒株的吞噬作用。
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Activation of macrophages for antimycobacterial activity.
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引用本文的文献

1
Mechanism of nitric oxide-dependent killing of Mycobacterium bovis BCG in human alveolar macrophages.人肺泡巨噬细胞中一氧化氮依赖性杀伤牛分枝杆菌卡介苗的机制
Infect Immun. 1997 Sep;65(9):3644-7. doi: 10.1128/iai.65.9.3644-3647.1997.
2
Response of Mycobacterium tuberculosis to reactive oxygen and nitrogen intermediates.结核分枝杆菌对活性氧和氮中间产物的反应。
Mol Med. 1996 Jan;2(1):134-42.
3
The role of T cell--macrophage interactions in tuberculosis.T细胞与巨噬细胞相互作用在结核病中的作用。
Springer Semin Immunopathol. 1988;10(4):337-58. doi: 10.1007/BF02053845.
4
Oxygen-independent killing by alveolar macrophages.肺泡巨噬细胞的非氧依赖性杀伤作用。
J Exp Med. 1986 May 1;163(5):1113-31. doi: 10.1084/jem.163.5.1113.
5
Attempts to characterize the mechanisms involved in mycobacterial growth inhibition by gamma-interferon-activated bone marrow macrophages.对γ-干扰素激活的骨髓巨噬细胞抑制分枝杆菌生长所涉及机制的研究尝试。
Infect Immun. 1988 Jun;56(6):1464-9. doi: 10.1128/iai.56.6.1464-1469.1988.
6
Mechanisms involved in mycobacterial growth inhibition by gamma interferon-activated bone marrow macrophages: role of reactive nitrogen intermediates.γ干扰素激活的骨髓巨噬细胞抑制分枝杆菌生长的机制：活性氮中间体的作用
Infect Immun. 1991 Sep;59(9):3213-8. doi: 10.1128/iai.59.9.3213-3218.1991.