Chensue S W, Shmyr-Forsch C, Weng A, Otterness I G, Kunkel S L
Department of Pathology, Veterans Administration Medical Center, Ann Arbor, Michigan.
J Leukoc Biol. 1989 Dec;46(6):529-37. doi: 10.1002/jlb.46.6.529.
The present study examined changes in lipopolysaccharide (LPS)-induced interleukin 1 (IL-1) and tumor necrosis factor (TNF) production by murine peritoneal macrophages during the chronic exudative response to Freund's complete adjuvant (CFA). Macrophages were isolated by peritoneal lavage and adherence at intervals over a 32 day period following i.p. injection of CFA. Optimal culture conditions for IL-1 and TNF production were predetermined, and it was found that IL-1 production was profoundly impaired at densities of above 150 cells/mm2, whereas TNF synthesis was more resistant to density effects. Using optimal conditions, we observed a sequential appearance of monokines. On day 0 there was minimal IL-1 production and no detectable TNF production. By days 4-7, IL-1 production reached maximum levels with a steady decline to baseline by day 32. TNF production steadily increased after day 2, reached maximal levels by days 16-20, and then partly declined by day 32. These findings were supported by kinetic analyses at specified days. When related to exudative events, it appeared that maximal IL-1 was associated with the recruitment stage of the reaction, whereas TNF production was associated with the established exudate. Immunohistochemical analysis revealed that TNF production could be related to the proportion of macrophages with cytoplasmic TNF expression. In contrast, IL-1 alpha and -1 beta expression was comparable among populations with 85-100% of cells showing cytoplasmic expression 6 hr after LPS stimulus. Whereas cytoplasmic IL-1 alpha persisted for the 18 hr study period, IL-1 beta disappeared from many adjuvant recruited cells. Our findings suggest that monokine production is orchestrated during macrophage recruitment and activation at sites of chronic inflammation.
本研究检测了在对弗氏完全佐剂(CFA)的慢性渗出反应过程中,脂多糖(LPS)诱导的小鼠腹腔巨噬细胞白细胞介素1(IL-1)和肿瘤坏死因子(TNF)产生的变化。腹腔注射CFA后,在32天的时间间隔内,通过腹腔灌洗和贴壁分离巨噬细胞。预先确定了IL-1和TNF产生的最佳培养条件,发现当细胞密度高于150个细胞/mm2时,IL-1的产生受到严重损害,而TNF的合成对密度效应更具抗性。在最佳条件下,我们观察到单核因子的顺序出现。在第0天,IL-1产生极少,未检测到TNF产生。到第4 - 7天,IL-1产生达到最高水平,到第32天稳步下降至基线。TNF产生在第2天后稳步增加,在第16 - 20天达到最高水平,然后到第32天部分下降。这些发现得到了特定天数的动力学分析的支持。当与渗出事件相关时,似乎最大的IL-1与反应的募集阶段相关,而TNF的产生与已形成的渗出物相关。免疫组织化学分析显示,TNF的产生可能与细胞质中表达TNF的巨噬细胞比例有关。相比之下,在LPS刺激6小时后,85 - 100%的细胞显示细胞质表达的群体中,IL-1α和 -1β的表达相当。虽然细胞质中的IL-1α在18小时的研究期间持续存在,但IL-1β在许多佐剂募集的细胞中消失。我们的发现表明,在慢性炎症部位巨噬细胞的募集和激活过程中,单核因子的产生是有组织的。