Crippen T L, Klasing K C, Hyde D M
Department of Anatomy, University of California, Davis, CA 95616, USA.
Pathobiology. 1998;66(6):293-301. doi: 10.1159/000028036.
During the course of inflammation, macrophages are highly influenced by their local environment and changes in the cytokine milieu. Exposure of macrophages to various factors during different phases of the inflammatory response may have a strong influence on the pattern of gene expression, which a macrophage exhibits. We examined how these mediators affect the regulation of the expression and production of cytokine-induced neutrophil chemoattractant (CINC). Our study demonstrates that CINC can be induced in bone marrow-derived macrophages by lipopolysaccharide, interleukin-1 beta, tumor necrosis factor-alpha (TNFalpha), and interferon-gamma/TNF alpha. These mediators are factors which a macrophage would be expected to encounter early in an inflammatory process. In contrast, transforming growth factor-beta (TGFbeta), which is expressed late in the inflammatory process during mesenchymal cell proliferation and tissue repair, did not induce detectable amounts of CINC and functioned to suppress CINC production stimulated by early inflammatory mediators. Suppression of CINC production occurred whether TGF beta was added simultaneously, 12 or 24 h prior to the stimulus.
在炎症过程中，巨噬细胞受到其局部环境和细胞因子环境变化的高度影响。在炎症反应的不同阶段，巨噬细胞暴露于各种因素可能会对巨噬细胞所表现出的基因表达模式产生强烈影响。我们研究了这些介质如何影响细胞因子诱导的中性粒细胞趋化因子（CINC）的表达和产生的调节。我们的研究表明，脂多糖、白细胞介素-1β、肿瘤坏死因子-α（TNFα）和干扰素-γ/TNFα可在骨髓来源的巨噬细胞中诱导CINC。这些介质是巨噬细胞在炎症过程早期可能遇到的因素。相比之下，在间充质细胞增殖和组织修复过程中炎症后期表达的转化生长因子-β（TGFβ）不会诱导可检测量的CINC，并且其作用是抑制早期炎症介质刺激的CINC产生。无论TGFβ是在刺激前同时添加、提前12小时还是24小时添加，都会发生CINC产生的抑制。
