(210k) Mucoid Switch Enables a Growth Advantage to Pseudomonas Aeruginosain Interfacial Environments

Balmuri, S., University of Pittsburgh
Waters, N., University of Pittsburgh
Niepa, T. H. R., University of Pittsburgh
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 can undergo pathoadaptation leading to a mucoid phenotype with unique material properties. We hypothesize that the mucoid switch provides a growth advantage to P. aeruginosa through the development of interfacial films with viscoelastic properties enabling colony restructuring and cell survival.In this study, we investigated the interfacial properties of films formed by non-mucoid (PANT) and mucoid (PASL) strains of P. aeruginosaisolated from CF patients. We used pendant drop elastometry to analyze the interfacial response of the films formed by PANT and PASL at hexadecane-water interfaces. The dynamic rheological properties of these films exposed to interfacial stresses demonstrated that the mucoid strains have a distinctive signature. When exposed to a constant strain, films of PASL exhibit more relaxation under compression than tension, while the perfect hysteresis behavior is achieved by PANT, which is characterized by a viscoelastic response conserved under both compression and tension. Wrinkling and shape analyses of the interfacial films elucidated that mucoid strain exhibits remarkable viscoelastic properties enabling remodeling of the living films through dissipation of compressive stresses. Microscopic analysis revealed that the interfacial films of PASL retained an intact cellular morphology compared to PANT, which harbor a large number of lysed cells. This indicates that the secretion of mucoid materials by PASL plays an important role in protecting the bacteria from interfacial stresses. Further characterization of biological materials will provide new insights toward the development of methods for controlling bacterial growth on biointerfaces.