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2016 ; 84
(12
): 3564-3574
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Cyclic di-AMP Released from Staphylococcus aureus Biofilm Induces a Macrophage
Type I Interferon Response
#MMPMID27736778
Gries CM
; Bruger EL
; Moormeier DE
; Scherr TD
; Waters CM
; Kielian T
Infect Immun
2016[Dec]; 84
(12
): 3564-3574
PMID27736778
show ga
Staphylococcus aureus is a leading cause of community- and nosocomial-acquired
infections, with a propensity for biofilm formation. S. aureus biofilms actively
skew the host immune response toward an anti-inflammatory state; however, the
biofilm effector molecules and the mechanism(s) of action responsible for this
phenomenon remain to be fully defined. The essential bacterial second messenger
cyclic diadenylate monophosphate (c-di-AMP) is an emerging pathogen-associated
molecular pattern during intracellular bacterial infections, as c-di-AMP
secretion into the infected host cytosol induces a robust type I interferon (IFN)
response. Type I IFNs have the potential to exacerbate infectious outcomes by
promoting anti-inflammatory effects; however, the type I IFN response to S.
aureus biofilms is unknown. Additionally, while several intracellular proteins
function as c-di-AMP receptors in S. aureus, it has yet to be determined if any
extracellular role for c-di-AMP exists and its release during biofilm formation
has not yet been demonstrated. This study examined the possibility that c-di-AMP
released during S. aureus biofilm growth polarizes macrophages toward an
anti-inflammatory phenotype via type I interferon signaling. DacA, the enzyme
responsible for c-di-AMP synthesis in S. aureus, was highly expressed during
biofilm growth, and 30 to 50% of total c-di-AMP produced from S. aureus biofilm
was released extracellularly due to autolytic activity. S. aureus biofilm
c-di-AMP release induced macrophage type I IFN expression via a STING-dependent
pathway and promoted S. aureus intracellular survival in macrophages. These
findings identify c-di-AMP as another mechanism for how S. aureus biofilms
promote macrophage anti-inflammatory activity, which likely contributes to
biofilm persistence.
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