Enhanced fatty acid biosynthesis by Sigma28 in stringent responses contributes to multidrug resistance and biofilm formation in .

The metabolic state of bacteria significantly contributes to their resistance to antibiotics; however, the specific metabolic mechanisms conferring antimicrobial resistance in remain largely understudied. Employing transcriptomic and non-targeted metabolomics, we characterized the metabolic reprogramming of when challenged with antibiotic agents. We observed a notable increase in both genetic and key proteomic components involved in fatty acid biosynthesis.

Antibiotic-induced ROS-mediated Fur allosterism contributes to resistance by inhibiting activation of and .

The increasing antibiotic resistance of primarily driven by genetic mutations poses a significant clinical challenge. Although previous research has suggested that antibiotics could induce genetic mutations in , the molecular mechanisms regulating the antibiotic induction remain unclear. In this study, we applied various techniques (e.

Quantified pathway mutations associate epithelial-mesenchymal transition and immune escape with poor prognosis and immunotherapy resistance of head and neck squamous cell carcinoma.

Background: Pathway mutations have been calculated to predict the poor prognosis and immunotherapy resistance in head and neck squamous cell carcinoma (HNSCC). To uncover the unique markers predicting prognosis and immune therapy response, the accurate quantification of pathway mutations are required to evaluate epithelial-mesenchymal transition (EMT) and immune escape. Yet, there is a lack of score to accurately quantify pathway mutations.

Aloe-emodin destroys the biofilm of Helicobacter pylori by targeting the outer membrane protein 6.

Biofilm formation is one of the most important factors causing drug resistance of Helicobacter pylori. Therefore, it is necessary to explore the mechanism underlying the biofilm formation and its eradication methods. The outer membrane proteins (OMPs) play important roles in the formation of bacterial biofilms and are considered the essential targets for new drug discovery.

The Quinone-Derived Small Molecule M5N32 Is an Effective Anti-Helicobacter pylori Agent Both In Vivo and In Vitro.

Background: Helicobacter pylori has become increasingly resistant to all commonly used clinical antibiotics. Therefore, new anti-H. pylori drugs need to be identified.