McCabe R E, Meagher S G, Mullins B T
Medical Service, Martinez VA Medical Center, California 94553.
J Infect Dis. 1991 Apr;163(4):912-5. doi: 10.1093/infdis/163.4.912.
Parenteral interferon-gamma (IFN-gamma) activates murine macrophages to inhibit Trypanosoma cruzi multiplication and diminishes parasitemia and mortality in acute infection. To investigate the role of endogenous IFN-gamma in acute infection, monoclonal antibody to IFN-gamma was injected intraperitoneally into mice. The 6250 neutralizing units given 24 and 96 h after infection reproducibly increased mortality (P less than .05). Histology sections showed markedly more nests of T. cruzi in treated mice. BALB/c, Swiss Webster, C57Bl/6, and C3H/HEN mice were susceptible to the effects of anti-IFN-gamma. Peritoneal macrophages from mice 4 days after infection and a single dose of 6250 units of anti-IFN-gamma had significantly reduced ability to inhibit T. cruzi multiplication. Multiple doses of anti-IFN-gamma delayed but did not prevent macrophage activation. These results indicate the critical role of endogenous IFN-gamma for macrophage activation and host defense against acute T. cruzi infection in mice.
肠外注射γ干扰素（IFN-γ）可激活小鼠巨噬细胞，抑制克氏锥虫增殖，并降低急性感染中的寄生虫血症和死亡率。为研究内源性IFN-γ在急性感染中的作用，将抗IFN-γ单克隆抗体腹腔注射到小鼠体内。在感染后24小时和96小时给予6250个中和单位可重复性地增加死亡率（P<0.05）。组织学切片显示，接受治疗的小鼠体内克氏锥虫巢明显更多。BALB/c、瑞士韦伯斯特、C57Bl/6和C3H/HEN小鼠均易受抗IFN-γ的影响。感染后4天的小鼠腹腔巨噬细胞和单剂量6250单位抗IFN-γ抑制克氏锥虫增殖的能力显著降低。多剂量抗IFN-γ可延迟但不能阻止巨噬细胞激活。这些结果表明内源性IFN-γ对小鼠巨噬细胞激活和宿主抵抗急性克氏锥虫感染起着关键作用。
