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首页> 外文期刊>Infection and immunity >Induction of murine gamma interferon production by lipopolysaccharide and interleukin-2 in Propionibacterium acnes-induced peritoneal exudate cells.
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Induction of murine gamma interferon production by lipopolysaccharide and interleukin-2 in Propionibacterium acnes-induced peritoneal exudate cells.

机译：脂多糖和白细胞介素2在痤疮丙酸杆菌诱导的腹膜渗出细胞中诱导鼠γ干扰素产生。

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Lipopolysaccharide (LPS) induces high levels of gamma interferon (IFN-gamma) in the circulation of mice pretreated with heat-killed Propionibacterium acnes. The following results were obtained in the present study. LPS, as well as interleukin-2 (IL-2), was also able to induce IFN-gamma in vitro in peritoneal exudate cells (PEC) from such mice. Splenocytes and lymph node cells from these mice or resident peritoneal cells from control mice produced trace or undetectable amount of IFN-gamma upon exposure to LPS. A synergistic effect on IFN-gamma induction was observed when LPS was added to a culture of PEC together with IL-2. Indomethacin augmented the induction of IFN-gamma by LPS or IL-2, and prostaglandin E2 reversed its effect. Deprivation of plastic-adherent or nylon wool-adherent cells abolished the induction by LPS or IL-2, whereas it did not affect that by concanavalin A. Culture supernatant of plastic-adherent cells incubated with LPS stimulated the nylon wool-nonadherent cells to produce IFN-gamma in the presence of IL-2, but interleukin-1 or phorbol myristic acetate did not replace the LPS-stimulated supernatant. The ability of PEC to produce IFN-gamma measured as a function of time after P. acnes injection increased in proportion to their natural killer (NK)-like activity against YAC-1 cells. Moreover, treatment of PEC with monoclonal anti-Thy-1 antibody or with anti-asialo GM1 antiserum plus complement eliminated the production of IFN-gamma and the NK-like activity simultaneously, whereas treatment with monoclonal anti-Lyt-2 antibody plus complement did not. These results suggest that IL-2 and some unidentified factor released from plastic-adherent cells by LPS stimulation cooperatively induce IFN-gamma production in activated, Thy-1- and asialo GM1-positive NK-like cells appearing in inflammatory reactions and that prostaglandin E2 regulates IFN-gamma production in these cells.
机译：脂多糖（LPS）在用热杀死的痤疮丙酸杆菌预处理的小鼠循环中诱导高水平的γ-干扰素（IFN-γ）。在本研究中获得以下结果。 LPS以及白介素2（IL-2）也能够在体外从此类小鼠的腹膜渗出细胞（PEC）中诱导IFN-γ。当暴露于LPS时，这些小鼠的脾细胞和淋巴结细胞或对照小鼠的常腹膜细胞会产生痕量或不可检测的IFN-γ。当将LPS与IL-2一起加入PEC培养物中时，观察到了对IFN-γ诱导的协同作用。消炎痛增强了LPS或IL-2对IFN-γ的诱导作用，前列腺素E2逆转了其作用。剥夺粘附塑料或尼龙毛的细胞消除了LPS或IL-2的诱导作用，而对伴刀豆球蛋白A的诱导没有影响。与LPS孵育的粘附塑料的培养上清液刺激了不粘附尼龙毛的细胞产生IL-2存在下的IFN-γ，但白介素-1或佛波醇肉豆蔻酸乙酸盐不能代替LPS刺激的上清液。注射痤疮丙酸杆菌后，PEC产生IFN-γ的能力随时间的变化与它们对YAC-1细胞的天然杀伤（NK）样活性成正比。此外，用单克隆抗Thy-1抗体或抗asialo GM1抗血清加补体治疗PEC可以同时消除IFN-γ的产生和NK样活性，而用单克隆抗Lyt-2抗体加补体治疗确实可以不。这些结果表明，IL-2和LPS刺激从塑性粘附细胞释放的一些未知因子协同诱导炎症反应中激活的Thy-1和无唾液GM1阳性NK样细胞中的IFN-γ产生，而前列腺素E2调节这些细胞中的IFN-γ产生。

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