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Hyaluronan Modulation Impacts Staphylococcus aureus Biofilm Infection.
Carolyn B Ibberson1, Corey P Parlet1, Jakub Kwiecinski1
1Department of Microbiology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA.
Infection and Immunity
|April 13, 2016
Summary
Staphylococcus aureus biofilms utilize hyaluronic acid (HA) for structural integrity. The enzyme hyaluronidase (HysA) degrades HA, reducing biofilm formation and infection spread.
Area of Science:
- Microbiology
- Biochemistry
- Pathogenesis
Background:
- Staphylococcus aureus is a major cause of persistent biofilm infections.
- Hyaluronic acid (HA), a component of mammalian tissues, promotes biofilm formation in pathogens.
Purpose of the Study:
- To investigate the role of HA in S. aureus biofilm development and infection.
- To determine the function of S. aureus hyaluronidase (HysA) in cleaving HA during infection.
Main Methods:
- Murine implant-associated infection model to observe HA accumulation.
- In vitro biofilm assays with HA and S. aureus strains (wild type and hysA mutant).
- Confocal microscopy to visualize HA within the biofilm matrix.
- Enzymatic assays using purified HysA and catalytically inactive variants.
- Histopathological analysis of infected tissues.
Main Results:
- HA was found to accumulate in S. aureus biofilms in vivo and in vitro.
- The hysA mutant exhibited increased biofilm biomass due to HA incorporation.
- Exogenous HysA effectively dispersed HA-containing biofilms.
- hysA mutant infections showed reduced dissemination and tissue inflammation in mice.
- HA contributed to synovial fluid aggregate formation, which HysA disrupted.
Conclusions:
- HA is an integral component of the S. aureus biofilm matrix.
- S. aureus HysA plays a critical role in cleaving HA, thereby limiting biofilm integrity and infection dissemination.
- Targeting HysA could be a therapeutic strategy against S. aureus biofilm infections.
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