Lipopolysaccharides (LPS；內毒素)為格蘭氏陰性菌細胞壁中的成份之一。當人體受到格蘭氏陰性菌嚴重感染時，細菌的LPS會經由血液侵犯人體，引發發燒、敗血性休克，甚至是器官衰竭等症狀。當細菌侵入時，由單核球分化而來的巨噬細胞會透過吞噬作用將這些危害人體的毒素吞入，裂解並消滅之，因此巨噬細胞在細菌引發的發炎反應中扮演著非常重要的角色。本文研究發現，在 Raw264.7 巨噬細胞株活化的過程中 LPS 可誘發 c-Src 表現量的增加。另外利用老鼠做為 model，抽取的 thioglycolate-elicited peritoneal macrophages (PEM) 在 LPS 處理後，也有 LPS-induced c-Src expression 的現象，也與 LPS 處理細胞造成第二階段蛋白 tyrosyl phosphorylation 增加的發現不謀而合。有趣的是，在 LPS 引發第一波短暫的蛋白的 tyrosyl phosphorylation 之後隨即加入 PP2 ，則細胞無論在第二階段中無論總蛋白 tyrosyl phosphorylation 的增加、COX-2蛋白表現量的上升、或一氧化氮的釋出上均有效受到抑制。最後，我們更證明了腹腔注射 LPS 老鼠的巨噬細胞較諸對照組，不但呈現活化而且其 c-Src 表現量也明顯增加。這意味著 LPS 誘發 c-Src 蛋白量的增加在巨噬細胞的活化上可能扮演一重要的角色。
Lipopolysaccharides (LPS) are cell wall components of most Gram-negative bacteria. During sereve Gram-negative bacterial infections, large amounts of LPS may be released into the blood stream and result in various pathophysiological symptoms such as fever, septic shock, and multi-organ failure. During bacterial infection, monocytes will differentiate into macrophages that can phagocytize the pathogens neutralize the toxins and play a critical role in inflammatory responses. In this study, we observed that LPS induced c-Src expression in Raw264.7 murine macrophage cell lines. Furthermore, we demonstrated that LPS induces c-Src expression in isolate thioglycolate-elicited peritoneal macrophages (PEM). In parallel with c-Src induction is the second wave increase of the total protein phosphorylation in LPS-treated Raw264.7 cells. Interestingly, the LPS-induced protein tyrosyl phosphorylation, COX-2 expression and NO production are aborogated in cells treated with PP2. Furthermore, we demonstrated that macrophages harvest from rats peritoneally injected LPS exhibits increase of c-Src expression as compared to those derived from PBS-injected control. Our study suggests that LPS-induced c-Src expression is a physiological event that might play an important role in macrophage activation.
