SpoT-mediated NapA upregulation promotes oxidative stress-induced Helicobacter pylori biofilm formation and confers multidrug resistance

Recently, there is increased incidence of drug-resistant infection. Biofilm formation confers multidrug resistance to bacteria. Moreover, it has been found that the formation of biofilm on the surface of gastric mucosa is an important reason for the difficulty of eradication of The mechanisms underlying biofilm formation have not been elucidated. Reactive oxygen species (ROS) released by the host immune cells in response to infection cannot effectively clear the pathogen. Moreover, the extracellular matrix of the biofilm protects the bacteria against ROS-mediated toxicity. This study hypothesized that ROS can promote biofilm formation and treatment with low concentrations of hydrogen peroxide (H O ) promoted this process The comparative transcriptome analysis of planktonic and biofilm-forming cells revealed that the expression of SpoT, a (p)ppGpp (guanosine 3'-diphosphate 5'-triphosphate and guanosine 3',5'-bispyrophosphate) synthetase/hydrolase, is upregulated in H O -induced biofilms and that knockout of inhibited biofilm formation. Additionally, this study examined the key target molecules involved in SpoT regulation using weighted gene co-expression network analysis. The analysis revealed that neutrophil-activating protein (NapA; HP0243) promoted H O -induced biofilm formation and conferred multidrug resistance. Furthermore, vitamin C exhibited anti- biofilm activity and downregulated the expression of These findings provide novel insight into the clearance of biofilms.