Abstract
Due to its ability to form biofilms on medical devices, Staphylococcus epidermidis has emerged as a major pathogen of nosocomial infections. In this study, we investigated the role of the two-component signal transduction system ArlRS in regulating S. epidermidis biofilm formation. An ArlRS-deficient mutant, WW06, was constructed using S. epidermidis strain 1457 as a parental strain. Although the growth curve of WW06 was similar to that of SE1457, the mutant strain was unable to form biofilms in vitro. In a rabbit subcutaneous infection model, sterile disks made of polymeric materials were implanted subcutaneously followed with inoculation of WW06 or SE1457. The viable bacteria cells of WW06 recovered from biofilms on the embedded disks were much lower than that of SE1457. Complementation of arlRS genes expression from plasmid in WW06 restored biofilm-forming phenotype both in vivo and in vitro. WW06 maintained the ability to undergo initial attachment. Transcription levels of several genes involved in biofilm formation, including icaADBC, sigB, and sarA, were decreased in WW06, compared to SE1457; and icaR expression was increased in WW06, detected by real-time reverse-transcription PCR. The biofilm-forming phenotype was restored by overexpressing icaADBC in WW06 but not by overexpressing sigB, indicating that ArlRS regulates biofilm formation through the regulation of icaADBC. Gel shift assay showed that ArlR can bind to the promoter region of the ica operon. In conclusion, ArlRS regulates S. epidermidis biofilm formation in an ica-dependent manner, distinct from its role in S. aureus.
Highlights
Staphylococcus epidermidis is an opportunistic pathogen that normally colonizes human skin and mucosal surfaces
Construction of an arlRS Gene-deficient Mutant Strain of S. epidermidis In S. epidermidis strain SE1457, the transduction systems (TCSs) arlRS consists of two genes, arlS and arlR, which share the same promoter and overlap by 4 bp
To investigate the function of arlRS in S. epidermidis biofilm formation, an ArlRS deficient mutant was constructed by replacing the arlS gene with an erythromycin-resistant cassette in the biofilm-forming SE1457 strain
Summary
Staphylococcus epidermidis is an opportunistic pathogen that normally colonizes human skin and mucosal surfaces. Over the past two decades, S. epidermidis has emerged as a major pathogen of nosocomial infections, infections involving indwelling medical device [1,2,3]. S. epidermidis pathogenesis is associated with its ability to colonize polymer surfaces to form multilayered biofilms, which impair the efficacy of antibiotic treatments and serve to protect the bacteria from the host immune system [4,5]. In S. epidermidis, whereas the TCSs Agr, LytSR and SaeRS are known to be involved in biofilm formation [15,16,17], the role of the ArlRS TCS remains unclear
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