Abstract
Both bacterial and host factors contribute to complicated bloodstream infection (BSI) caused by Staphylococcus aureus including methicillin-resistant S. aureus (MRSA). One bacterial factor that may affect the persistence of S. aureus in complicated BSI is reduced susceptibility to the innate immune defence peptide LL-37. LL-37 susceptibility among S. aureus isolates causing uncomplicated and complicated BSI was investigated. Following incubation with 2.5 μg/ml LL-37 for 1 h, the mean percentage survival was 67.6% and 74.9% for isolates causing uncomplicated and complicated BSI, respectively. Reduced LL-37 susceptibility may contribute to the persistence of S. aureus in complicated BSI.
Highlights
The clinical outcome of bloodstream infection (BSI) caused by Staphylococcus aureus is variable and both bacterial and host innate immune factors may contribute to the clinical course of infection
Among S. aureus clinical isolates causing complicated and uncomplicated BSI there was a wide variation in susceptibility to killing by LL-37 under the assay conditions used
Overall, S. aureus isolates causing uncomplicated BSI were more susceptible to killing by LL37 than isolates causing complicated BSI but this difference was not statistically significant (p = 0.48, Student’s t-test) (Figure 1(a))
Summary
The clinical outcome of bloodstream infection (BSI) caused by Staphylococcus aureus is variable and both bacterial and host innate immune factors may contribute to the clinical course of infection. The innate immune system acts as the first line of defence against microorganisms such as S. aureus and cationic anti-microbial peptides (CAMPs) are an important component of the innate immune response [1]. S. aureus has evolved mechanisms that confer reduced susceptibility to CAMPS such as LL-37, allowing it to evade this important component of innate immunity. These mechanisms are poorly understood, a number of potential factors have been identified and include aureolysin, which inactivates LL-37 and both polysaccharide intracellular adhesion (PIA) and fibrinogen-binding protein (fnBP) which have been shown to reduce susceptibility to LL-37 [4,5,6]. Increased surface charge, achieved by the incorporation of D-alanine into teichoic acid or of lysine into phosphati-
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