Cell子刊：靶向抑制大肠杆菌毒力因子，改善酒精肝

Core Viewpoint - The study highlights the significant correlation between the virulence factor KpsM in Escherichia coli and the mortality rate of patients with alcohol-associated liver disease, suggesting that targeted inhibition of KpsM could be a promising approach to improve patient prognosis [2][3][9]. Group 1: Research Findings - The presence of KpsM in the genome of Escherichia coli is associated with higher mortality rates in patients suffering from alcohol-associated liver disease [3][7]. - KpsM-positive Escherichia coli exacerbates alcohol-induced liver disease in mouse models [5][7]. - KpsM mediates the transport of capsular polysaccharides to the cell surface, allowing KpsM-positive Escherichia coli to evade phagocytosis by Kupffer cells in the liver, leading to its spread [5][7]. Group 2: Therapeutic Implications - The small molecule C7, which inhibits KpsM-dependent capsular formation, has been shown to alleviate alcohol-induced liver disease in mice [6][7]. - The study provides evidence that precision targeting of the pathogenic factor KpsM is a promising method for improving the prognosis of patients with alcohol-associated liver disease [9].