Abstract: Biofilms are aggregates of single-cell organisms that are stuck to each other by a matrix of polymer and protein. Establishment of a biofilm infection creates a reservoir of pathogens that tolerate antibiotics and evade the immune system, can prevent healing, and have the potential to spread and cause sepsis. The most common biofilm-forming bacteria isolated from chronic wounds are Staphylococcus aureus and Pseudomonas aeruginosa. Burkholderia pseudomallei is a biofilm-forming pathogen that is endemic to tropical areas such as southeast Asia, and is spreading to other areas including the southern United States. Type I collagen is the most abundant protein in all vertebrates, including humans. We grow biofilms of P. aeruginosa, S. aureus, and B. pseudomallei in concentrations of 0%, 10%, and 20% collagen that includes the concentration of collagen found in burns, wounds, and other anatomical sites of biofilm infection. Growth with collagen changes both the mechanical and microstructural properties of the biofilm.

Neutrophils are phagocytic white blood cells that are “first responders” to infection and densely surround biofilm aggregates in wounds and other soft-tissue environments. We incubate freshly-isolated human neutrophils with biofilms for one hour and then measure the percentage of neutrophils that have engulfed bacteria. We find that incorporation of Type I collagen into P. aeruginosa, S. aureus, and B. pseudomallei biofilms hinders phagocytosis of biofilm bacteria by human neutrophils, by up to a factor of two. Enzymatic degradation of collagen using collagenase reverses these effects, increasing biofilm susceptibility to neutrophils.

Early results suggest that collagen likely protects biofilms through the physical properties, both microstructural and mechanical, that growth with collagen induces in the biofilm. These results also show that materials made by the infected host can play significant roles in stabilizing and protecting biofilm infections. Targeting host materials and their interactions within the biofilm matrix has the potential to provide a pathogen-agnostic approach to treating biofilm infections.

Bio: Vernita Gordon is a Professor of Physics at the University of Texas at Austin, associated with the Center for Nonlinear Dynamics, the Institute for Cellular and Molecular Biology, and the LaMontagne Center for Infectious Disease. Prof. Gordon received her BSc in Physics and her PhD from Harvard University in 2003. She went on to do postdocs at University of Edinburgh, Scotland, and University of Illinois at Urbana-Champaign, including as a Cystic Fibrosis Foundation Postdoctoral Fellow, before joining the faculty at UT Austin 2010. There she has built a very successful experimental biophysics group focused on how cells interact with each other and with their environment, with a special focus on biofilms including their mechanical properties and immune system effects. Among other honors, Dr. Gordon was elected a Fellow of the American Physical Society in 2023. Dr. Gordon also holds Trull Centennial Professorship and Elizabeth B. Gleeson Professorship fellowships. In addition, Dr. Gordon has received several teaching awards and was previously a Provost’s Teaching Fellow.