IDENTIFICATION OF CYTOKINES WHICH ENHANCE (CSF-1, IL-3) OR RESTRICT (IFN-GAMMA) GROWTH OF INTRAMACROPHAGE LISTERIA-MONOCYTOGENES

IDENTIFICATION OF CYTOKINES WHICH ENHANCE (CSF-1, IL-3) OR RESTRICT (IFN-GAMMA) GROWTH OF INTRAMACROPHAGE LISTERIA-MONOCYTOGENES
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DOI:
10.1016/0165-2478(91)90158-7
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发表时间:
1991-03-01
期刊:
影响因子:
4.4
通讯作者:
GREGG, EO
GREGG, EO
中科院分区:
医学3区
文献类型:
--
作者:
DENIS, M;GREGG, EO

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通过贴壁分离小鼠腹膜巨噬细胞,并在存在或不存在选定的细胞因子的情况下评估它们的杀菌活性。未经处理的巨噬细胞对链球菌的杀灭作用不强,在感染后的头2小时表现出中等杀灭能力,并允许微生物在此后(最多9小时)进行生长。用10-100U/ml的干扰素-γ对细胞进行预处理,可使巨噬细胞在9小时的观察期内产生持续的李斯特菌杀灭活性,每单层的李斯特氏菌落数减少2对数。单独用肿瘤坏死因子-α冲击细胞并不能增强杀灭微生物的活性,但肿瘤坏死因子-α能增强干扰素-γ诱导的杀菌活性,当两种细胞因子同时存在时,导致高水平的杀灭。相反,用白介素3(IL-3)或集落刺激因子-1(CSF-1)预处理的巨噬细胞被发现对李斯特菌的生长更宽容。IL-3和CSF-1均不能阻断干扰素-γ诱导的杀菌活性。此外,IL-3和CSF-1都不影响巨噬细胞在李斯特菌感染后发生呼吸爆发的能力,这是通过体外感染后的过氧化氢释放来判断的。总之,这些结果表明,不同的细胞因子可能对细胞内微生物的生长具有相反的影响,体内细胞因子产生的平衡可能决定受感染宿主的抵抗力或敏感性。
Murine peritoneal macrophages were isolated by adherence and their listericidal activity assessed in the presence or absence of selected cytokines. Untreated macrophages were not highly listericidal, showing moderate killing in the first 2 h after infection, and allowed progressive microbial growth thereafter (up to 9 h). Pre-treatment of cells with 10 to 100 U/ml of IFN-gamma allowed macrophages to develop sustained listericidal activity for the 9-h observation period, with a 2-log reduction of Listeria CFU per monolayer. Pulsing of cells with TNF-alpha alone did not result in enhanced microbicidal activity but TNF-alpha potentiated IFN-gamma-induced listericidal activity, resulting in high levels of killing when both cytokines were present. Conversely, macrophages pre-treated with interleukin-3 (IL-3) or colony-stimulating factor-1 (CSF-1) were found to be much more permissive for Listeria growth. Neither IL-3 nor CSF-1 abrogated IFN-gamma-induced listericidal activity. Moreover, neither IL-3 nor CSF-1 had any effect on the ability of macrophages to develop a respiratory burst following Listeria infection, as judged by H2O2 release following in vitro infection. Overall, these results suggest that different cytokines may have opposing effects on intracellular microbial growth, and that the balance of cytokine production in vivo may determine the resistance or susceptibility of the infected host.