人體在病原菌入侵時，會啟動免疫系統。巨噬細胞在人體的免疫反應當中扮演著十分重要的角色；其除了能吞噬病原菌之外，還能誘發後天免疫系統，產生更專一的免疫反應。脂多醣，為格蘭氏陰性菌細胞壁的成分之ㄧ，可以為巨噬細胞表面的TLR-4認識，活化巨噬細胞並誘發發炎。丁酸鈉為腸道內細菌代謝纖維素的產物之ㄧ，先前的文獻指出，丁酸鈉具有降低腸道內皮細胞發炎及抑制大腸直腸癌的形成的能力。在本篇的報告中，我們發現巨噬細胞受到脂多醣刺激後，細胞內的c-Src和Eps8會隨著巨噬細胞的活化而表現量增加；但在加入丁酸鈉之後，則此誘發的情形明顯的被抑制下來。另外，c-Src和Eps8已分別被報導參與細胞的移行，而我們發現在處理丁酸鈉之後，受脂多醣活化的巨噬細胞移動能力也隨之下降。由此可知，在丁酸鈉抑制巨噬細胞產生發炎的過程中，會抑制巨噬細胞內c-Src和Eps8的表現進而抑制了巨噬細胞的移動。本篇報告為丁酸鈉抑制巨噬細胞活化提出了新的思維及證據。
Immune system will be turned on when human is infected by pathogens and macrophages are important players. In addition to phagocytose pathogens，macrophages can also induce adaptive immunity to perform more specific responses. Lipopolysaccharide，an outer membrane component of Gram-negative bacteria，is known to be recognized by TLR4 on the surface of macrophages，and elicit inflammation. Sodium butyrate is a fermentation end-product of dietary fiber by bacteria in intestines. Previous reports indictate that sodium butyrate can repress the inflammation of intestinal epithelial cells and prevent the formation of colon cancer. In this study，we discover that butyrate can inhibit LPS-induced c-Src and Eps8. Since c-Src and Eps8 are implicated in macrophage migration，their downregulation mediated by butyrate results in suppressed motility of LPS-activated macrophages. According to these evidences，we believe that sodium butyrate can repress expressions of c-Src and Eps8，and also inhibit migration ability of macrophages in the process of anti-inflammation of sodium butyrate. Our report reveal a new opinion and evidences about that sodium butyrate can repress LPS-induced macrophage activation.
