| Autor: |
Zhou X; Center for Nonlinear Dynamics, The University of Texas at Austin, 2515 Speedway, Stop C1610, Austin, Texas 78712-11993, USA.; Interdisciplinary Life Sciences Graduate Program, Norman Hackerman Building, 100 East 24th St., NHB 4500, Austin, Texas 78712, USA., Wells MJ; Center for Nonlinear Dynamics, The University of Texas at Austin, 2515 Speedway, Stop C1610, Austin, Texas 78712-11993, USA.; Department of Physics, The University of Texas at Austin, 2515 Speedway, C1600, Austin, Texas 78712-1192, USA., Gordon VD; Center for Nonlinear Dynamics, The University of Texas at Austin, 2515 Speedway, Stop C1610, Austin, Texas 78712-11993, USA.; Interdisciplinary Life Sciences Graduate Program, Norman Hackerman Building, 100 East 24th St., NHB 4500, Austin, Texas 78712, USA.; Department of Physics, The University of Texas at Austin, 2515 Speedway, C1600, Austin, Texas 78712-1192, USA.; LaMontagne Center for Infectious Disease, The University of Texas at Austin, Neural Molecular Science Building, 2506 Speedway, Stop A5000, Austin, Texas 78712, USA. |
| Abstrakt: |
Biofilms are communities of microbes embedded in a matrix of extracellular polymeric substances (EPS). Matrix components can be produced by biofilm organisms and can also originate from the environment and then be incorporated into the biofilm. For example, we have recently shown that collagen, a host-produced protein that is abundant in many different infection sites, can be taken up into the biofilm matrix, altering biofilm mechanics. The biofilm matrix protects bacteria from clearance by the immune system, and some of that protection likely arises from the mechanical properties of the biofilm. Pseudomonas aeruginosa and Staphylococcus aureus are common human pathogens notable for forming biofilm infections in anatomical sites rich in collagen. Here, we show that the incorporation of Type I collagen into P. aeruginosa and S. aureus biofilms significantly hinders phagocytosis of biofilm bacteria by human neutrophils. However, enzymatic treatment with collagenase, which breaks down collagen, can partly or entirely negate the protective effect of collagen and restore the ability of neutrophils to engulf biofilm bacteria. From these findings, we suggest that enzymatic degradation of host materials may be a potential way to compromise biofilm infections and enhance the efficacy of the host immune response without promoting antibiotic resistance. Such an approach might be beneficial both in cases where the infecting species is known and also in cases wherein biofilm components are not readily known, such as multispecies infections or infections by unknown species. |
