674686 event 1715601559 1715601869 <![CDATA[The mechanics and microstructures of biofilms impact phagocytosis by immune cells]]> Vernita Gordon has been on the faculty at the University of Texas at Austin since 2010.  Her research group studies the interplay of physics and biology in bacterial biofilms, with a long-term goal of finding cases where physical properties can be targeted to prevent or treat biofilm disease.  Her PhD students and postdocs have gone on to a wide range of jobs in industry and academia.  Her work has been funded by the National Science Foundation, the National Institutes of Health, the Cystic Fibrosis Foundation, the Air Force Office of Scientific Research, and the Human Frontiers Science Program.  She was elected a Fellow of the American Physical Society in 2023.  

]]> Thus, a population of microbes in a biofilm state have viscoelastic properties that do not exist for the same population of bacteria that are suspended as individual cells in liquid culture.  Biofilms also have biological properties that arise from the biofilm state – these include heightened tolerance of antibiotics and the inability of the immune system to clear infections in the form of biofilms, even though the same population of bacteria as individual cells would be very susceptible to antibiotics and easily engulfed by the immune system.  As a result, biofilm infections are a major and increasing problem in healthcare in a wide range of scenarios.

 

The aggregates comprising biofilm infections are an order of magnitude larger in size than phagocytic immune cells.  Therefore, for biofilm microbes to be cleared by phagocytosis, they must be separated from the biofilm.  This must involve mechanical and structural compromise of the biofilm.  Using abiotic gels as models to recreate biofilm mechanics, we have shown that the success of human neutrophils at engulfing things out of the gel is impacted by gel viscoelasticity and toughness.  More recently, we have grown biofilms from three important human pathogens (Pseudomonas aeruginosa, Staphylococcus aureus, and Burkholderia pseudomallei) under conditions that mimic key physiological conditions.  Differences in the mechanics and microstructure arise from the presence of collagen and calcium ions are linked to changes in the efficacy of human neutrophils at engulfing bacteria from the biofilm.  Treatment of key matrix components, that takes into account chances induced by physiological components, can significantly increase the ability of neutrophils to engulf biofilm bacteria.

 

In future, we hope to extend this to a roadmap for designing specific treatments that compromise biofilm mechanics and microstructure to make them more susceptible to clearance by the immune system.

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