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体液免疫与免疫功能正常宿主中嗜肺军团菌肺内生长的调节

Humoral immunity and regulation of intrapulmonary growth of Legionella pneumophila in the immunocompetent host.

作者信息

Brieland J K, Heath L A, Huffnagle G B, Remick D G, McClain M S, Hurley M C, Kunkel R K, Fantone J C, Engleberg C

机构信息

Unit for Laboratory Animal Medicine, University of Michigan, Ann Arbor 48109, USA.

出版信息

J Immunol. 1996 Dec 1;157(11):5002-8.

PMID:8943407
Abstract

The potential role of humoral immunity in regulating intrapulmonary growth of Legionella pneumophila in the immunocompetent host was investigated using a murine model of Legionnaires' disease. Intratracheal inoculation of A/J mice with a virulent strain of L. pneumophila (10(6) bacteria per mouse) resulted in the recruitment of B lymphocytes into the lung and the development of anti-L. pneumophila Ab. Opsonization of L. pneumophila in vitro with anti-L. pneumophila-specific mAb resulted in a significant decrease in intrapulmonary growth of the bacteria at 24 to 72 h postinfection. Transmission electron microscopic analysis of lung tissue from L. pneumophila- infected mice demonstrated that while there was no significant difference between phagocytosis of the unopsonized and opsonized L. pneumophila by alveolar macrophages at 24 h postinfection, phagocytosis of opsonized bacteria by alveolar mononuclear phagocytic cells was significantly enhanced at 48 h postinfection. Depletion of A/J mice of complement before intratracheal inoculation of opsonized L. pneumophila (10(6) bacteria per mouse) did not significantly alter intrapulmonary growth of L. pneumophila. These results suggest that anti-L. pneumophila Ab, produced during replicative L. pneumophila lung infections, may regulate intrapulmonary growth of L. pneumophila in the immunocompetent host by decreasing the viability of extracellular L. pneumophila and by enhancing phagocytosis of the bacteria by alveolar mononuclear phagocytic cells by a complement-independent mechanism.

摘要

利用军团病小鼠模型,研究了体液免疫在免疫功能正常宿主中调节嗜肺军团菌肺内生长的潜在作用。给A/J小鼠气管内接种一株强毒嗜肺军团菌(每只小鼠10⁶个细菌),导致B淋巴细胞募集到肺内,并产生抗嗜肺军团菌抗体。用抗嗜肺军团菌特异性单克隆抗体在体外对嗜肺军团菌进行调理,导致感染后24至72小时细菌在肺内的生长显著减少。对嗜肺军团菌感染小鼠的肺组织进行透射电子显微镜分析表明,虽然感染后24小时肺泡巨噬细胞对未调理和调理后的嗜肺军团菌的吞噬作用没有显著差异,但感染后48小时肺泡单核吞噬细胞对调理后细菌的吞噬作用显著增强。在气管内接种调理后的嗜肺军团菌(每只小鼠10⁶个细菌)之前,去除A/J小鼠的补体,并未显著改变嗜肺军团菌在肺内的生长。这些结果表明,在嗜肺军团菌肺部感染复制过程中产生的抗嗜肺军团菌抗体,可能通过降低细胞外嗜肺军团菌的活力,并通过补体非依赖机制增强肺泡单核吞噬细胞对细菌的吞噬作用,来调节免疫功能正常宿主中嗜肺军团菌的肺内生长。

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