Colloquium-Physics Department - Vernita Gordon (University of Texas at Austin)

About this event

Host material incorporated into biofilm matrices alters the biofilm's viscoelastic mechanics and microstructure and helps protect against clearance by the immune system

Biofilms are aggregates of single-cell organisms that are stuck to each other by a matrix of polymers, including polysaccharides, proteins, and nucleic acids. Biofilms are viscoelastic materials, possessing both solid-like (elastic) and fluid-like (viscous) properties. They are also highly inhomogeneous, non-continuum materials, with micron-sized bacteria intermingled with polymers that can have widths of 2-100nm and lengths of tens of microns or more. Biofilms can form infections that tolerate antibiotics and evade the immune system. Indeed, most chronic bacterial infections are made by bacterial biofilms. Most of these infections grow in anatomical locations which are rich in Type I collagen, which is the most abundant protein in all vertebrates, including humans. We have recently shown, using a mouse model for chronic wounds, that biofilms grown in a living animal have different viscoelastic properties than biofilms grown in an artificial environment, and that incorporation of collagen from the infected host can account for most of this difference. This demonstrates that understanding the role of collagen, made by the host, has strong potential clinical importance. For three different types of important biofilm-forming human pathogens, we have used microrheology and electron microscopy to show that they can incorporate collagen from their environment and that this changes both their viscoelastic mechanics and their microstructure. Furthermore, we have shown that incorporation of collagen can help to protect biofilms from the immune system. 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 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.