Altering the Interfacial Properties of Mixed Films of Pseudomonas Aeruginosa and Staphylococcus Aureus with N-Acetyl Cysteine and Cysteamine

Chronic lung infection with bacterial biofilms is one of the leading causes of death in cystic fibrosis (CF) patients. Among many species colonizing the lung airways, Pseudomonas aeruginosa and Staphylococcus aureus are two of the most prevalent pathogens responsible for recalcitrant infections. These pathogens contribute to a mechanically robust biofilm that is difficult to eradicate using methods such as lung lavage and airway clearance techniques. Disrupting agents such as glycoside hydrolase-based compounds are commonly employed to target and break down the biofilm matrix components, and subsequently increase cell susceptibility to antibiotics. In this study, we evaluated the effects of N-acetyl cysteine (NAC) and Cysteamine (CYST) in disrupting the interfacial bacterial films by targeting different components of the extracellular polymeric substances (EPS). Our results showed that the biofilm architectures were compromised by both disrupting agents. The loss of structural integrity of the interfacial bacterial films was characterized using pendant drop tensiometry and scanning electron microscopy. We further assessed the effects of competition or cooperative behavior on the mechanics of mixed interfacial films of S. aureus and P. aeruginosa. Viscoelastic properties revealed that the interfacial biofilms lost their strength after the treatment with disrupting agents for a duration of 6 h. These effects were profound in the wild type and mucoid P. aeruginosa biofilms compared to S. aureus. Cocultured films of S. aureus with wild type P. aeruginosa showed a reduced strength before and after the treatment while cocultures of S. aureus with mucoid P. aeruginosa showed increased strength which decreased as a result of the treatments with the disrupting agents. Overall, our results will provide new insights towards the development of treatment method against interfacial biofilms as those seen in lungs of CF patients.