HOST DEFENSES IN MURINE MALARIA - ANALYSIS OF PLASMODIAL INFECTION-CAUSED DEFECTS IN MACROPHAGE MICROBICIDAL CAPACITIES
HOST DEFENSES IN MURINE MALARIA - ANALYSIS OF PLASMODIAL INFECTION-CAUSED DEFECTS IN MACROPHAGE MICROBICIDAL CAPACITIES
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DOI：
10.1128/iai.31.1.396-407.1981
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发表时间：
1981-01-01
影响因子：
3.1
通讯作者：
MURPHY, JR
中科院分区：
文献类型：
--
作者：
MURPHY, JR
巨噬细胞依赖性的兼性细胞内细菌的杀伤作用明显受损的明显红细胞约氏疟原虫或伯氏疟原虫感染的小鼠。约氏疟原虫感染不仅能破坏正常动物巨噬细胞的杀菌能力，而且能破坏活化巨噬细胞的杀菌能力。疟原虫感染并没有改变脾和肝对单核细胞增生李斯特菌的静脉注射挑战的吸收，但在注射后数小时内，在疟疾小鼠的组织中发现了显著增强的细菌生长。这些证据证实了这样一种观点，即疟疾小鼠的巨噬细胞对细菌的吸收是正常的，但与正常小鼠不同，疟疾小鼠无法杀死细菌。疟原虫感染引起的巨噬细胞杀微生物能力的缺陷可以通过静脉内注射大量非复制异源颗粒（即，杀死的细菌、绵羊红细胞）。在显性红细胞疟疾期间产生的颗粒的摄取可能是与疟疾相关的巨噬细胞杀菌能力缺陷的原因。
Macrophage-dependent killing of facultative intracellular bacteria was markedly impaired by overt erythrocytic Plasmodium yoelii or P. berghei infection of mice. P. yoelii infection was capable of ablating not only the macrophage microbicidal capacity of normal animals but also the bactericidal capacities of activated macrophage. The uptake by spleen and liver of an i.v. challenge of Listeria monocytogenes was not altered by plasmodial infection, but within hours of injection markedly enhanced bacterial growth was found in tissues of malarious mice. The evidence gives credence to the view that the uptake of bacteria by macrophages of malarious mice was normal but that malarious mice, unlike normal mice, were unable to kill the bacteria. The plasmodial infection-caused defect in macrophage microbicidal capacity could be partially mimicked by the i.v. injection of large numbers of nonreplicating heterologous particles (i.e., killed bacteria, sheep erythrocytes). The uptake of particles generated during overt erythrocytic malaria may be responsible for the malaria-associated defects in macrophage bactericidal capacity.