Abstract

The colonization of Staphylococcus aureus, especially methicillin-resistant S. aureus (MRSA), has a detrimental effect on the respiratory care of pediatric patients with cystic fibrosis (CF). In addition to being resistant to multiple antibiotics, S. aureus also has the ability to form biofilms, which makes the infection more difficult to treat and eradicate. In this study, we examined the ability of S. aureus strains isolated from pediatric patients with CF to form biofilms. We screened a transposon mutant library of MRSA and identified a putative cobalt transporter ATP binding domain (cbiO) that is required for biofilm formation. We discovered that deleting cbiO creating a cbiO null mutant in CFSa36 (an MRSA strain isolated from a patient with cystic fibrosis) significantly hinders the ability of CFSa36 to form biofilm. The complementation of cbiO restored the ability of the cbiO deletion mutant to generate biofilm. Interestingly, we revealed that incorporating extra copper ions to the chemically defined medium (CDM) complemented the function of cbiO for biofilm formation in a dose-dependent manner, while the addition of extra iron ions in CDM enhanced the effect of cbiO null mutation on biofilm formation. In addition, neither the addition of certain extra amounts of copper ions nor iron ions in CDM had an impact on bacterial growth. Taken together, our findings suggest that cbiO mediates biofilm formation by affecting the transportation of copper ions in the MRSA CFSa36 strain. This study provides new insights into the molecular basis of biofilm formation by S. aureus.

Highlights

  • Staphylococcus aureus is an important opportunistic human pathogen that causes a variety of diseases

  • We identified that a cobalt transporter ATP binding domain is important for biofilm formation by screening a Nebraska Transposon mutant library of CA-methicillin-resistant S. aureus (MRSA)

  • We observed that different S. aureus isolates from patients with cystic fibrosis (CF) exhibited a distinct capacity of invading host cells [7] and led us to question whether these strains are able to form biofilms

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Summary

Introduction

Staphylococcus aureus is an important opportunistic human pathogen that causes a variety of diseases. MRSA is a critical pathogen that causes infection in patients with cystic fibrosis (CF). Macrocolonies of MRSA are often found embedded within the mucinous layer and forming biofilms. This biofilm presence can clearly limit antibiotic killing due to (a) reduced antibiotic concentrations reaching bacteria due to the presence of polymerizable mucopolysaccharides on the biofilms, (b) entrapment of metabolically inactive bacteria within the biofilm, and (c) the accumulation of bacterial cells within the biofilm facilitatig horizontal gene transfer responsible for antibiotic resistence [3]. The ability of MRSA to form biofilms compounded with multidrug resistance significantly decreases the efficacy of standard drug therapy and leads to poor outcomes in CF patients [4]

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