Czermak B J, Lentsch A B, Bless N M, Schmal H, Friedl H P, Ward P A
Department of Trauma Surgery, University of Freiburg Medical School, Freiburg/Breisgau, Germany.
Am J Pathol. 1999 May;154(5):1513-24. doi: 10.1016/S0002-9440(10)65405-3.
Complement plays an important role in many acute inflammatory responses. In the current studies it was demonstrated that, in the presence of either C5a or sublytic forms of the complement-derived membrane attack complex (MAC), rat alveolar macrophages costimulated with IgG immune complexes demonstrated synergistic production of C-X-C (macrophage inflammatory protein-2 and cytokine-induced neutrophil chemoattractant) and C-C (macrophage inflammatory protein-1alpha and monocyte chemoattractant-1) chemokines. In the absence of the costimulus, C5a or MAC did not induce chemokine generation. In in vivo studies, C5a and MAC alone caused limited or no intrapulmonary generation of chemokines, but in the presence of a costimulus (IgG immune complexes) C5a and MAC caused synergistic intrapulmonary generation of C-X-C and C-C chemokines but not of tumor necrosis factor alpha. Under these conditions increased neutrophil accumulation occurred, as did lung injury. These observations suggest that C5a and MAC function synergistically with a costimulus to enhance chemokine generation and the intensity of the lung inflammatory response.
补体在许多急性炎症反应中发挥重要作用。在当前研究中已证实，在存在C5a或补体衍生的膜攻击复合物（MAC）的亚溶解形式时，用IgG免疫复合物共刺激的大鼠肺泡巨噬细胞会协同产生C-X-C（巨噬细胞炎性蛋白-2和细胞因子诱导的中性粒细胞趋化因子）和C-C（巨噬细胞炎性蛋白-1α和单核细胞趋化因子-1）趋化因子。在没有共刺激的情况下，C5a或MAC不会诱导趋化因子的产生。在体内研究中，单独的C5a和MAC导致肺内趋化因子的产生有限或不产生，但在存在共刺激（IgG免疫复合物）的情况下，C5a和MAC导致肺内C-X-C和C-C趋化因子的协同产生，但不产生肿瘤坏死因子α。在这些条件下，中性粒细胞积累增加，肺损伤也会发生。这些观察结果表明，C5a和MAC与共刺激协同发挥作用，以增强趋化因子的产生和肺部炎症反应的强度。
