Adib-Conquy M, Petit A F, Marie C, Fitting C, Cavaillon J M
Unité d'Immuno-Allergie, Institut Pasteur, 28 rue Dr Roux, 75015 Paris, France.
Int Immunol. 1999 May;11(5):689-98. doi: 10.1093/intimm/11.5.689.
IL-10 is a well-known immunosuppressive and/or anti-inflammatory cytokine. However, we report in vitro experimental studies in which IL-10 primed leukocytes and led to an enhanced production of tumor necrosis factor (TNF) upon further stimulation by lipopolysaccharide (LPS). Monocytes and peripheral blood mononuclear cells (PBMC) prepared from whole blood maintained for 20 h at 37 degrees C in the presence of recombinant human IL-10 had an enhanced capacity to produce TNF in response to LPS. In addition to TNF, LPS-induced IL-6 and spontaneous IL-1ra production were also enhanced. When isolated PBMC were first cultured for 20 h in the presence of IL-10 on Teflon to prevent adherence, washed to remove IL-10 and then further cultured in plastic dishes for an additional 20 h in the presence of LPS or IL-1beta, an enhanced release of TNF was observed. This was not the case when PBMC were pre-cultured in plastic multidishes in the presence of IL-10. TNF mRNA expression induced by LPS was decreased when the pre-treatment of PBMC with IL-10 was performed on plastic, whereas this was not the case when cells were pre-cultured with IL-10 on Teflon. Furthermore, NFkappaB translocation following LPS activation was higher after IL-10 pre-treatment on Teflon than on plastic. Interestingly, an enhanced frequency of CD16 and CD68(+) cells among the CD14(+) cells was observed in the presence of IL-10, independently of the pre-culture conditions of the PBMC. Altogether, these results indicate that the IL-10-induced up-regulation of cytokine production depends on the prevention of monocyte adherence by red cells in the whole blood assays or by cultures of PBMC on Teflon. In contrast, the adherence parameter has no effect on the IL-10-induced modulation of some monocyte surface markers.
白细胞介素-10（IL-10）是一种众所周知的免疫抑制和/或抗炎细胞因子。然而，我们报道了体外实验研究，其中IL-10预处理白细胞，并在脂多糖（LPS）进一步刺激后导致肿瘤坏死因子（TNF）产生增强。在重组人IL-10存在下于37℃保存20小时的全血制备的单核细胞和外周血单个核细胞（PBMC）对LPS产生TNF的能力增强。除了TNF，LPS诱导的IL-6和自发性IL-1ra产生也增强。当分离的PBMC首先在特氟龙上于IL-10存在下培养20小时以防止黏附，洗涤以去除IL-10，然后在LPS或IL-1β存在下于塑料培养皿中再培养20小时时，观察到TNF释放增强。当PBMC在IL-10存在下于塑料多孔培养皿中预培养时则不是这种情况。当在塑料上用IL-10预处理PBMC时，LPS诱导的TNF mRNA表达降低，而当细胞在特氟龙上用IL-10预培养时则不是这种情况。此外，在特氟龙上用IL-10预处理后，LPS激活后NFκB易位高于在塑料上。有趣的是，在IL-10存在下，无论PBMC的预培养条件如何，在CD14(+)细胞中观察到CD16和CD68(+)细胞的频率增加。总之，这些结果表明，IL-10诱导的细胞因子产生上调取决于全血检测中红细胞对单核细胞黏附的预防或PBMC在特氟龙上的培养。相反，黏附参数对IL-10诱导的一些单核细胞表面标志物的调节没有影响。
