Mechanism and role of phagocytosis of dying cells and microbes

1)SR-BI介导睾丸支持细胞凋亡的机制及作用。睾丸体细胞支持细胞吞噬凋亡的生精细胞后，产生未知因子(S)，使生精细胞分化为精子。通过对Sertoli细胞的蛋白质组学分析，筛选出一个候选蛋白，并对其一级结构进行了鉴定。我们发现，在吞噬过程中，该因子的表达在转录水平得到了刺激。我们已经建立了该因子的基因敲除小鼠，我们将检测该因子在小鼠精子发生中的作用。2)TLR-JNK途径在细菌存活巨噬细胞中的作用金黄色葡萄球菌依赖Toll样受体TLR2诱导小鼠腹腔巨噬细胞JNK磷酸化。这种墨水途径的激活抑制了巨噬细胞中超氧化物的产生，从而使吞噬的金黄色葡萄球菌得以在巨噬细胞中存活。3)巨噬细胞吞噬流感病毒感染细胞的作用流感病毒感染的细胞产生巨噬细胞激活因子，增强病毒感染细胞的巨噬细胞吞噬功能，这依赖于病毒感染和细胞凋亡。该因子是热不稳定物质，因为它在热处理后失去了活性。

1) Mechanism and role of SR-BI-mediated apoptotic spermatogenic cells by Sertoli cells in the testis. After phagocytosis of apoptotic spermatogenic cells, testicular somatic Sertoli cells produced unknown factor(s) by which spermatogenic cells could differentiate into spermatozoa. To identify the factor, we selected one candidate protein by proteome analysis of Sertoli cells and identified its primary structure. We found that the expression of the factor was stimulated in transcriptional level during phagocytosis. We have been generating knockout mice of the factor, and we are going to examine the role of the factor on spermatogenesis in mice.2) Role of TLR-JNK pathway on bacterial survival in macrophages Staphylococcus aureus induced JNK phosphorylation in mouse peritoneal macrophages depending on toll-like receptor TLR2. This activation of INK pathway caused inhibition of superoxide production in the macrophages, and this allowed engulfed S. aureus to survive in the macrophages.3) Role of phagocytosis of influenza virus-infected cells by macrophages Influenza virus-infected cells produced macrophage-activating factor that enhance macrophage phagocytosis of virus-infected cells depending on both virus infection and apoptosis. This factor would be heat-labile material since it lost the activity after heat-treatment.