Truyens C, Angelo-Barrios A, Torrico F, Van Damme J, Heremans H, Carlier Y
Laboratory of Parasitology, Faculty of Medicine, University of Brussels, Belgium.
Infect Immun. 1994 Feb;62(2):692-6. doi: 10.1128/iai.62.2.692-696.1994.
Trypanosoma cruzi infection of mice triggered endogenous production of interleukin-6 (IL-6) during the ascending phase of parasitemia. Injections of anti-IL-6 monoclonal antibody in infected mice at the time of the serum IL-6 peak paradoxically increased IL-6 levels to 60- to 80-fold those in infected mice receiving unrelated immunoglobulins. This early and transient increase in circulating IL-6 levels modified neither the immunoglobulin nor T. cruzi-specific antibody levels of immunoglobulin G1 (IgG1), IgG2a, IgG3, IgM, IgA, and IgE isotypes or the final outcome of infection nor the blood or tissular parasite levels. However, it tended to delay mortality of mice and to increase the levels of the acute-phase protein serum amyloid P component.
克氏锥虫感染小鼠会在寄生虫血症上升阶段引发白细胞介素-6(IL-6)的内源性产生。在血清IL-6达到峰值时给感染小鼠注射抗IL-6单克隆抗体,结果却出人意料地使IL-6水平升高至接受无关免疫球蛋白的感染小鼠的60至80倍。循环IL-6水平的这种早期短暂升高既未改变免疫球蛋白水平,也未改变免疫球蛋白G1(IgG1)、IgG2a、IgG3、IgM、IgA和IgE同种型的克氏锥虫特异性抗体水平,也未改变感染的最终结果以及血液或组织中的寄生虫水平。然而,它往往会延迟小鼠的死亡,并增加急性期蛋白血清淀粉样P成分的水平。