Feng H M, Walker D H
Department of Pathology, University of Texas Medical Branch, Galveston 77555-0609.
Am J Pathol. 1993 Oct;143(4):1016-23.
How the host defenses control rickettsiae in the cytosol of nonphagocytic host cells, where they are not exposed to antibodies or phagocytes, has posed a difficult question. Rickettsia conorii infection of a mouse fibroblast cell line was inhibited in a dose-dependent manner by nitrogen oxide synthesized by eukaryotic host cells stimulated by interferon-gamma or tumor necrosis factor-alpha. L-arginine was the source of the nitric oxide as demonstrated by competitive inhibition by NG-monomethyl-L-arginine. Nitric oxide synthesis required host cell protein synthesis and had an approximately 48-hour lag phase following cytokine stimulation. At low doses of interferon-gamma and tumor necrosis factor-alpha, which had no detectable response as single agents, dramatic synergistic nitric oxide synthesis and antirickettsial effects were observed.
在非吞噬性宿主细胞的胞质溶胶中，立克次氏体不会接触到抗体或吞噬细胞，宿主防御系统如何控制立克次氏体一直是个难题。γ干扰素或肿瘤坏死因子α刺激真核宿主细胞合成的一氧化氮，以剂量依赖的方式抑制了小鼠成纤维细胞系的康氏立克次体感染。NG-单甲基-L-精氨酸的竞争性抑制证明L-精氨酸是一氧化氮的来源。一氧化氮的合成需要宿主细胞蛋白质合成，并且在细胞因子刺激后有大约48小时的延迟期。在低剂量的γ干扰素和肿瘤坏死因子α单独使用时没有可检测到的反应，但却观察到了显著的协同一氧化氮合成和抗立克次体作用。
