Crippen T L, Riches D W, Hyde D M
Department of Anatomy, Physiology and Cell Biology, University of California, Davis 95616, USA.
Pathobiology. 1998;66(1):24-32. doi: 10.1159/000027991.
The production of cytokine-induced neutrophil chemoattractant (CINC) by functionally diverse mouse bone-marrow-derived macrophages was determined. Studies showed that beta1,3-glucan, IL-beta, TNFalpha and IFNgamma/TNFalpha induced expression and production of CINC in macrophages while neither IFNgamma nor TGFbeta alone induced detectable CINC expression. Pretreatment or simultaneous treatment of macrophages with TGFbeta resulted in suppression of CINC protein production. These studies demonstrate that IFNgamma and TNFalpha, found early during the inflammatory response, induce production of CINC, as well as induce macrophages into a cytocidal state that are capable of killing transformed cells, parasites and bacteria, and recruiting neutrophils. In contrast, TGFbeta, found during reparative stages of the inflammatory response, suppressed production of CINC, while inducing the development of inflammatory macrophages that are capable of producing lysosomal enzymes, enhanced endocytosis and ingestion of particulate matter and function to scavenge debris, debride tissue and stimulate repair.
测定了功能多样的小鼠骨髓源性巨噬细胞产生细胞因子诱导的中性粒细胞趋化因子（CINC）的情况。研究表明，β1,3-葡聚糖、白细胞介素-β、肿瘤坏死因子α以及干扰素γ/肿瘤坏死因子α可诱导巨噬细胞表达和产生CINC，而单独的干扰素γ或转化生长因子β均不能诱导可检测到的CINC表达。用转化生长因子β预处理或同时处理巨噬细胞会导致CINC蛋白产生受到抑制。这些研究表明，在炎症反应早期发现的干扰素γ和肿瘤坏死因子α可诱导CINC的产生，还能诱导巨噬细胞进入具有杀细胞作用的状态，这种状态下巨噬细胞能够杀死转化细胞、寄生虫和细菌，并募集中性粒细胞。相比之下，在炎症反应修复阶段发现的转化生长因子β可抑制CINC的产生，同时诱导炎性巨噬细胞的发育，这些炎性巨噬细胞能够产生溶酶体酶、增强内吞作用和对颗粒物的摄取，并起到清除碎片、清创组织和刺激修复的作用。
