Oswald I P, Dozois C M, Petit J F, Lemaire G
Laboratoire Associé INRA/ENVT, Toulouse, France.
Infect Immun. 1997 Apr;65(4):1364-9. doi: 10.1128/iai.65.4.1364-1369.1997.
Trehalose dimycolate (TDM), a glycolipid present in the cell wall of Mycobacterium spp., is a powerful immunostimulant. TDM primes murine macrophages (Mphi) to produce nitric oxide (NO) and to develop antitumoral activity upon activation with low doses of lipopolysaccharide (LPS). In this study, we investigated the ability of TDM to induce interleukin 12 (IL-12) and the role of this cytokine in TDM-induced activation of murine Mphi. RNA isolated from peritoneal exudate cells (PEC) collected at different times after TDM injection was used to determine IL-12 (p35 and p40 subunits) and gamma interferon (IFN-gamma) mRNA levels by semiquantitative reverse transcriptase-PCR. Constitutive expression of IL-12p35 was observed in PEC from untreated as well as from TDM-injected mice. In contrast, expression of the IL-12p40 subunit was almost undetectable in control PEC but was dramatically upregulated in PEC from TDM-injected mice. IL-12p40 expression peaked at 8 h and subsided to baseline levels at 39 h postinjection. TDM was also able to induce IFN-gamma expression; however, kinetics of induction of IFN-gamma was different from that of IL-12p40. Maximal levels of IFN-gamma mRNA were reached by 24 h and did not return to baseline by 4 days. In addition, pretreatment of mice with neutralizing monoclonal antibodies directed against IL-12 (C15.6.7 and C15.1.2) blocked IFN-gamma mRNA induction in PEC from TDM-treated mice. We further determined if the induction of IL-12 and/or IFN-gamma contributes to the in vivo priming effect of TDM on peritoneal Mphi. TDM-injected mice were treated in vivo with anti-IL-12 or anti-IFN-gamma (XMG.1.6) monoclonal antibodies. TDM-primed Mphi were then activated in vitro with LPS and tested for their ability to produce NO and to develop cytostatic activity toward cocultivated L1210 tumor cells. Priming of Mphi by TDM was completely blocked by in vivo neutralization of either IL-12 or IFN-gamma as demonstrated by an absence of tumoricidal activity and NO production by TDM-elicited Mphi in the presence of LPS. Taken together our results show that TDM, a defined molecule from M. tuberculosis, induces in vivo production of IL-12. Moreover, synthesis of IL-12 mediates TDM priming of mouse peritoneal Mphi through IFN-gamma induction.
海藻糖二分枝菌酸酯(TDM)是分枝杆菌属细胞壁中的一种糖脂,是一种强大的免疫刺激剂。TDM可使小鼠巨噬细胞(Mphi)致敏,使其在低剂量脂多糖(LPS)激活后产生一氧化氮(NO)并发挥抗肿瘤活性。在本研究中,我们研究了TDM诱导白细胞介素12(IL-12)的能力以及该细胞因子在TDM诱导的小鼠Mphi激活中的作用。从TDM注射后不同时间收集的腹腔渗出细胞(PEC)中分离的RNA,用于通过半定量逆转录聚合酶链反应测定IL-12(p35和p40亚基)和γ干扰素(IFN-γ)mRNA水平。在未处理小鼠以及TDM注射小鼠的PEC中均观察到IL-12p35的组成性表达。相比之下,IL-12p40亚基的表达在对照PEC中几乎检测不到,但在TDM注射小鼠的PEC中显著上调。IL-12p40表达在注射后8小时达到峰值,并在39小时后降至基线水平。TDM也能够诱导IFN-γ表达;然而,IFN-γ的诱导动力学与IL-12p40不同。IFN-γ mRNA的最大水平在24小时达到,并且在4天内未恢复到基线。此外,用针对IL-12的中和单克隆抗体(C15.6.7和C15.1.2)预处理小鼠可阻断TDM处理小鼠的PEC中IFN-γ mRNA的诱导。我们进一步确定IL-12和/或IFN-γ的诱导是否有助于TDM对腹腔Mphi的体内致敏作用。给TDM注射的小鼠体内注射抗IL-12或抗IFN-γ(XMG.1.6)单克隆抗体。然后用LPS在体外激活TDM致敏的Mphi,并测试其产生NO的能力以及对共培养的L1210肿瘤细胞产生细胞抑制活性的能力。如在LPS存在下TDM诱导的Mphi缺乏杀肿瘤活性和NO产生所证明的,通过体内中和IL-12或IFN-γ,TDM对Mphi的致敏作用被完全阻断。我们的结果共同表明,TDM(一种来自结核分枝杆菌的特定分子)可在体内诱导IL-12的产生。此外,IL-12的合成通过IFN-γ诱导介导TDM对小鼠腹腔Mphi的致敏作用。