| Description |
High-alcohol-producing K. pneumoniae (HiAlc Kpn) is a novel cause of nonalcoholic fatty liver disease(NAFLD), which can produce excess endogenous alcohol using carbon sources such as glucose in the gut of the patient. The role of glucose in HiAlc Kpn response to environmental stresses, such as antibiotics is still not clear. In this study, we found that glucose could enhance the resistance of HiAlc Kpn to polymyxins. On the one hand, glucose inhibited the expression of crp in HiAlc Kpn, and then promoted the production of capsular polysaccharide (CPS). The increased CPS promoted the resistance of HiAlc Kpn to polymyxins. On the other hand, glucose maintained higher ATP when HiAlc Kpn was treated by polymyxins, and ATP consumption is possible mechanism by which polymyxins kill bacteria. It is worth noting that both addition of cAMP and inhibition of glycolytic pathway and tricarboxylic acid cycle can effectively reverse the induction of polymyxins resistance by glucose. Finally, glucose-induced polymyxin resistance was found to be universal in K. pneumoniae, not just in HiAlc Kpn. Our work demonstrating the mechanism by which glucose induces polymyxins resistance in K. pneumoniae lays the groundwork for developing effective treatments for the NAFLD caused by HiAlc Kpn. |
