Florentin I, Nolibe D, Giroud J P
IPSN, DPS, Laboratoire de Toxicologie des Transuraniens, Bruyères Le Chatel, France.
Int J Exp Pathol. 1991 Feb;72(1):83-95.
A non-immunological acute inflammatory reaction, induced in rats by intrapleural injection of calcium pyrophosphate microcrystals, decreased natural killer activity of lung intracapillary leucocytes (LICL), and, to a lesser extent, of spleen cells. NK activity was significantly depressed as early as 2 h after pleurisy induction, maximally suppressed at 72 h (when the inflammation had resolved) and returned to near-normal values by day 10. This decrease in NK activity was demonstrated using YAC-I lymphoma cells and syngeneic fibrohistiocytoma (P77) cells, as targets. The inhibition of NK activity of LICL was accompanied by an impaired destruction of P77 tumour cells injected i.v. 3 days after the onset of pleurisy. This was shown by an increase in the number of radiolabelled tumour cells surviving in the lungs at 24 h and of tumour nodules developed in lung parenchyma at 3 weeks. Suppression of NK activity was not due to a decrease in the proportion of large granular lymphocytes (LGL) in the LICL population. Suppressor macrophages may be involved, at least in part, since a partial restoration of LICL cytotoxicity was obtained after depletion of plastic-adherent cells. The effect of inflammation was reproduced in normal rats by injecting inflammatory serum or PGE2, suggesting a possible role of circulating mediators.
通过向大鼠胸腔内注射焦磷酸钙微晶诱导的非免疫性急性炎症反应，降低了肺毛细血管内白细胞（LICL）的自然杀伤活性，对脾细胞的活性也有一定程度的降低。早在胸膜炎诱导后2小时，NK活性就显著降低，在72小时（炎症消退时）受到最大程度的抑制，并在第10天恢复到接近正常的值。使用YAC-I淋巴瘤细胞和同基因纤维组织细胞瘤（P77）细胞作为靶标，证实了NK活性的这种降低。LICL的NK活性受到抑制的同时，静脉注射P77肿瘤细胞后其破坏功能也受损。这表现为胸膜炎发作3天后，肺部24小时内存活的放射性标记肿瘤细胞数量增加，以及3周后肺实质中形成的肿瘤结节增多。NK活性的抑制并非由于LICL群体中大颗粒淋巴细胞（LGL）比例的降低。至少部分原因可能涉及抑制性巨噬细胞，因为去除贴壁细胞后，LICL的细胞毒性得到了部分恢复。通过注射炎性血清或前列腺素E2在正常大鼠中重现了炎症的作用，提示循环介质可能发挥了作用。
