吞噬感染与非感染凋亡粒细胞对人巨噬细胞的活化具有不同影响  

Divergent effects of phagocytosis of infected versus uninfected apoptotic neutrophils on activation of human macrophages

作　　者：龙敏[1] 冯永红[2] 龙北国[1] 付涌水 郑利民[2] 

机构地区：[1]南方医科大学微生物教研室,广州510515 [2]中山大学生命科学院生化系,广州510275 [3]广州市中心血站

出　　处：《中华微生物学和免疫学杂志》2004年第11期883-886,共4页Chinese Journal of Microbiology and Immunology

基　　金：国家自然科学基金资助项目 ( 3 0 3 7160 0 ) ;广东省自然科学基金资助项目 ( 0 3 162 0 )

摘　　要：目的　探讨感染与非感染诱导的凋亡中性粒细胞对人巨噬细胞 (MΦ)活性的影响。方法　用大肠杆菌 (E .coli)或金黄色葡萄球菌 (S .aureus)感染中性粒细胞 ,或经紫外线照射 ,以诱导其凋亡 ,观察吞噬这些凋亡细胞对人MΦ活性的影响。结果　吞噬照射诱导的凋亡粒细胞通过降低TNF α和增加TGF β来抑制MΦ活性。与此相反 ,吞噬感染所致的凋亡细胞可明显增加MΦ的TNF α产量并上调CD6 4 (FcγRⅠ )的表达。结论　粒细胞凋亡是调控免疫和炎症反应的一个重要机制。在炎症早期 ,粒细胞凋亡多由病原感染所致 ,吞噬这些细胞可激活MΦ而有助于控制病原 ;一旦病原被清除 ,在感染灶的多余粒细胞发生凋亡 ,吞噬这些非感染凋亡细胞可抑制MΦ活性 。Objective To explore the effect of bacterial infected versus uninfected-apoptotic neutrophils on the activity of human macrophages. Methods Both gram-negative and gram-positive bacteria E.coli and (S.aureus) were used to induce neutrophil apoptosis, then these pathogen-induced apoptotic neutrophils were ingested by human macrophages. As a control, uninfected-apoptotic neutrophils induced by UV irradiation were fed to macrophages. The production of cytokines TNF-α, TGF-β and IL-10 by macrophages and CD64 (FcγRⅠ) expression on macrophages surface were assayed. Results In contrast to ingestion of uninfected-apoptotic neutrophils, phagocytosis of bacteria-induced apoptotic cells caused MΦ to markedly increase production of the proinflammatory cytokine TNF-α but not the anti-inflammatory cytokine TGF-β. MΦ markedly increased FcγRⅠ expression after they ingested bacteria-induced, but not uninfected, -apoptotic neutrophils. Conclusion These opposing effects of infected-and uninfected -apoptotic neutrophils on MΦ activation might represent a novel mechanism that regulates host response to infection by control of pathogens at an early stage of infection, and later by avoiding tissue damage through removal of excess uninfected neutrophils. [

关 键 词：吞噬 凋亡细胞 感染 中性粒细胞 人巨噬细胞 诱导 炎症 E.COLI 调控 大肠杆菌 

分 类 号：R392[医药卫生—免疫学] R733[医药卫生—基础医学]