Different biofilm types contribute to resistance of Staphylococcus epidermidis against uptake by macrophages

Abstract number: P1897

Rohde H., Schommer N., Hentschke M., Ruckdeschel K., Aepfelbacher M.

Objectives: Formation of adherent multi cellular aggregates is the key mechanism involved in Staphylococcus epidermidis virulence in device associated infections. Aside from polysaccharide intercellular adhesin PIA, accumulation associated protein Aap and extracellular matrix binding protein Embp act as intercellular adhesins, mediating S. epidermidis biofilm accumulation. The aim of this study was to characterize structural features of PIA-, Aap-, and Embp-mediated S. epidermidis biofilms in more detail and to evaluate, by using well characterized S. epidermidis strain pairs, their specific contribution to biofilm-related S. epidermidis immune escape.

Results: PIA-dependent biofilms were characterized by densely packed bacteria, embedded in a PIA containing extracellular matrix. In sharp contrast, neither Aap- nor Embp-mediated biofilms featured a significant extracellular matrix. Despite this marked difference, PIA-, Aap-, and Embp-mediated biofilms protected S. epidermidis with similar efficiency against up-take by J774.A1 macrophages. The reduced phagocytic up-take was likewise associated with a significantly reduced NF-kappaB and AP-1 activation and Il-1b production compared to macrophage responses to biofilm-negative S. epidermidis strains not expressing the respective intercellular adhesins. Thus, interference of S. epidermidis biofilm formation with phagocytosis is due to over-all reduced phagocyte activation. More-over, contact with biofilm forming S. epidermidis also induced a reduction in macrophage's LPS responsiveness, suggesting biofilm-related induction of anti-inflammatory host cell events.

Conclusions: Our results not only demonstrate that independent mechanisms of biofilm formation are similar effective in protecting S. epidermidis from phagocytic up-take, but point towards specific events during S. epidermidis – macrophage interactions which interfere with phagocyte activation. As these result in failure to take up and eradicate S. epidermidis a detailed elucidation of the involved mechanisms could open new directions for development of therapeutic strategies to combat S. epidermidis infections.

Session Details

Date: 10/04/2010
Time: 00:00-00:00
Session name: Abstracts 20th European Congress of Clinical Microbiology and Infectious Diseases
Location: Vienna, Austria, 10 - 13 April 2010
Presentation type:
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