Hiding in Plain Sight: Interplay between Staphylococcal Biofilms and Host Immunity

Tyler D Scherr,John M Morrison,Tammy Kielian,Cortney E Heim

doi:10.3389/fimmu.2014.00037

Tyler D Scherr, John M Morrison + Show 2 more

Open Access

https://doi.org/10.3389/fimmu.2014.00037

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Abstract

Staphylococcus aureus and Staphylococcus epidermidis are notable for their propensity to form biofilms on implanted medical devices. Staphylococcal biofilm infections are typified by their recalcitrance to antibiotics and ability to circumvent host immune-mediated clearance, resulting in the establishment of chronic infections that are often recurrent in nature. Indeed, the immunomodulatory lifestyle of biofilms seemingly shapes the host immune response to ensure biofilm engraftment and persistence in an immune competent host. Here, we provide a brief review of the mechanisms whereby S. aureus and S. epidermidis biofilms manipulate host–pathogen interactions and discuss the concept of microenvironment maintenance in infectious outcomes, as well as speculate how these findings pertain to the challenges of staphylococcal vaccine development.

Highlights

Staphylococcus aureus and Staphylococcus epidermidis are highly opportunistic pathogens and a major cause of nosocomial and community-associated infections [1,2,3,4]
Most medical deviceassociated biofilm infections are caused by S. epidermidis and S. aureus, and both species can establish biofilms on native host surfaces, such as infective endocarditis and osteomyelitis [9,10,11]
Our laboratory has shown that macrophages associated with S. aureus biofilms both in vitro and in vivo have decreased inducible nitric oxide synthase concomitant with increased Arg1 expression, as well as attenuated cytokine and chemokine production [6, 43, 44]

Summary

Introduction

Staphylococcus aureus and Staphylococcus epidermidis are highly opportunistic pathogens and a major cause of nosocomial and community-associated infections [1,2,3,4]. While both staphylococcal species harbor multiple virulence factors, they are capable of biofilm formation, which represents a communal virulence determinant to circumvent immune-mediated clearance and establish persistent infection [5,6,7,8]. These innate leukocyte responses, coupled with complement activation, usually ensure the successful clearance of planktonic staphylococcal infections in an immune competent host.

Results

Conclusion