Phillips W A, Hamilton J A
Department of Medicine, University of Melbourne, Royal Melbourne Hospital, Parkville, Victoria, Australia.
J Cell Physiol. 1990 Aug;144(2):190-6. doi: 10.1002/jcp.1041440203.
Several cytokines have previously been shown to prime macrophages for enhanced release of oxygen radicals in response to subsequent stimulation. We now demonstrate that the presence of the macrophage-specific colony stimulating factor-1 (CSF-1) inhibits the priming of murine macrophages by a variety of agents including tumor necrosis factor alpha, granulocyte/macrophage colony stimulating factor, interferon-gamma, and bacterial lipopolysaccharide. CSF-1 is also able to reduce the respiratory burst in the absence of priming. Our results indicate that CSF-1 is a potent negative regulator of the macrophage respiratory burst which acts to oppose the priming (enhancing) action of macrophage activating agents. We propose that CSF-1 may have a potentially important and previously unrecognized, role as a physiological regulator which restricts or terminates the activation of macrophages in order to prevent an uncontrolled inflammatory reaction.
先前已表明，几种细胞因子可使巨噬细胞致敏，以增强其对后续刺激产生氧自由基的释放。我们现在证明，巨噬细胞特异性集落刺激因子-1（CSF-1）的存在可抑制多种因子对小鼠巨噬细胞的致敏作用，这些因子包括肿瘤坏死因子α、粒细胞/巨噬细胞集落刺激因子、干扰素-γ和细菌脂多糖。CSF-1在未致敏的情况下也能够减少呼吸爆发。我们的结果表明，CSF-1是巨噬细胞呼吸爆发的有效负调节因子，其作用与巨噬细胞激活剂的致敏（增强）作用相反。我们提出，CSF-1可能作为一种生理调节因子具有潜在的重要且以前未被认识到的作用，它限制或终止巨噬细胞的激活，以防止不受控制的炎症反应。
