Mupirocin enhances the biofilm formation of Staphylococcus epidermidis in an atlE-dependent manner.

The pathogenicity of Staphylococcus epidermidis is largely attributed to its exceptional ability to form biofilms. Here, we report that mupirocin, an antimicrobial agent widely used for staphylococcal decolonization and anti-infection, strongly stimulates the biofilm formation of S. epidermidis. Although the polysaccharide intercellular adhesin (PIA) production was unaffected, mupirocin significantly facilitated extracellular DNA (eDNA) release by accelerating autolysis, thereby positively triggering cell surface attachment and intercellular agglomeration during biofilm development. Mechanistically, mupirocin regulated the expression of genes encoding for the autolysin AtlE as well as the programmed cell death system CidA-LrgAB. Critically, through gene knockout, we found out that deletion of atlE, but not cidA or lrgA, abolished the enhancement of biofilm formation and eDNA release in response to mupirocin treatment, indicating that atlE is required for this effect. In Triton X-100 induced autolysis assay, mupirocin treated atlE mutant displayed a slower autolysis rate compared with the wild-type strain and complementary strain. Therefore, we concluded that subinhibitory concentrations of mupirocin enhance the biofilm formation of S. epidermidis in an atlE dependent manner. This induction effect could conceivably be responsible for some of the more unfavourable outcomes of infectious diseases.

The Value of Rivaroxaban Combined with Ticagrelor in Antithrombotic Therapy after PCI in Patients with Nonvalvular Atrial Fibrillation with Acute Coronary Syndrome.

Objective: Based on a retrospective cohort study, to investigate the value of rivaroxaban combined with ticagrelor in antithrombotic therapy after PCI in patients with nonvalvular atrial fibrillation with acute coronary syndrome. Methods: A total of 60 patients from January 2019 to May 2021 accepted therapy with antithrombotic therapy after PCI. The patients treated with ticagrelor were set as the control group, and those given rivaroxaban combined with ticagrelor were set as the research group. The curative effect, myocardial level, TIMI blood flow grade, platelet aggregation rate, and the incidence of cardiovascular events were taken from the comparisons. Results: The research group's therapeutic impact was superior to the control group's therapeutic impact, and the value was higher. After treatment, the myocardial levels of the two groups decreased, and the levels of troponin I, creatine kinase isoenzyme, and hypersensitive C-reactive protein in the research group were greatly less than those in the control group, and the difference was statistically significant (P < 0.05). After operation, the TIMI blood flow classification in the experimental group was better than that in the control group, and the difference was statistically significant (P < 0.05). The experimental group's platelet aggregation incidence was considerably lower than the control group's platelet aggregation incidence at 0.5 and 2 hours following surgery, and the difference was statistically significant (P < 0.05). The incidence of acute myocardial infarction, cardiogenic death, and intractable angina pectoris in the research group was significantly lower than that in the control group. Conclusion: Rivaroxaban combined with ticagrelor in the treatment of nonvalvular atrial fibrillation with acute coronary syndrome after percutaneous coronary intervention; the TIMI blood flow grade is better than ticagrelor, which is of great significance to reduce mortality and has high safety in clinical application.