摘要
目的：观察免疫活性细胞的相互作用及其对FNF－α生成的影响。方法：分离人中性粒细胞（polymorphonuclearleukocytes，PMN）并与PMA刺激分化为单核细胞样细胞的U937细胞在不同条件下共同培养。结果：在LPS作用下U937细胞可产生大量TNF－α。PMN在相同条件下并不产生INF－α。将PMN与U937细胞共同培养可抑制U937细胞TNF－α的生成。PMN的抑制作用呈数量依赖性。将两种细胞共处于同一培养体系中并用0．4μm的滤网分开使其不能直接接触，U937细胞产生TNF－α的能力恢复至无PMN时的85％以上。一氧化氮供体硝普钠可轻微提高U937细胞产生TNF－α的能力。但提高的幅度在有或无PMN存在的条件下均相同，与无硝普钢的对照组比较无明显差异（P＞0．05）。经鼠诱导型一氧化氮合酶基因转染的U937对细胞表达一氧化氮合酶的活性，所产生的内源性一氧化氮对PMN的抑制作用无影响。结论：提示PMN并非TNF－α生成细胞。PMN对单核细胞TNF－α的生成有抑制性调节作用。这种抑制作用的机制可能与一氧化氮信息传导通路无关。
AIM: To investigate the interaction between immunoactive cells and TNF -α production. METHODS:phorbol myristate acetate(PMA) differentiated U937 cells were cocultured with human polymorphonuclear leukocytes (PMN)in the presence of LPS. The supernatants of cell culture were collected and TNF -α was assayed with EIISA.RESULTS:U937 cells treated with PMA differentited to monocyte -like cells and produced large amotmt of TNF - αin the presence of LPS. Human PMN did not produce detectable amount of TNF -α in the same condition. Increasing numbers of PMN decreased U937 cell TNF -α secretion in a dose dependent manner. Separation of PMN from U937 cells by a 0. 4 μp filter insert in the co-culture system restored TNF -α release by > 85%. Sodium nitroprusside slightly increased TNF - α secretion by PMA differentiated U937 cells to a similar extet whether in the absence or presence of 5×10°PMN but there was no statistic significance when compared to the cells without sodium nitroprusside treatment (P >0. 05). U937 cells transfected with mouse macrophage inducible nitric oxide synthase (NOS) gene expressed NOS activity. However, this endogenously produced NO did not affect PMN mediated inhibition of TNF - α secretion in transfected U937 cells. CONCLUSIONS: The results indicated that PMN is not likely a source of TNF - α producing cells. PMN downregulated TNF -α production by human pyagocytic cells. The mechanism of PMN inhibition seemed independent to the nitric oxide signaling pathway.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1999年第9期777-780,共4页
Chinese Journal of Pathophysiology
基金
国家自然科学基金!39670309
卫生部科学基金
