Abstract
Anti-microbial peptides are produced at outer and inner surfaces by epithelia and innate immune cells in response to bacterial infection. Staphylococcus aureus is an enterotoxin producing, Gram-positive pathogen, which is a major cause of soft tissue infections and life-threatening bacteremia and sepsis. Here we show that (i) skin T cells in chronic wounds infected with S. aureus express interleukin-26 (IL-26) in situ, (ii) staphylococcal enterotoxins (SE) trigger IL-26 expression in T cell lines and primary skin T cells, and (iii) IL-26 triggers death and inhibits biofilm formation and growth of S. aureus. Thus, we provide novel evidence that IL-26 is an anti-microbial peptide produced by T cells in response to SE. Accordingly, we propose that IL-26 producing T cells take part in the innate immune response to SE producing S. aureus and thus play a novel role in the primary innate immune defense in addition to their classical role in adaptive immunity.
Highlights
Staphylococcus aureus is a major cause of lifethreatening infections such as bacteremia, sepsis, and endocarditis and account for approximately 19,000 deaths per year in the United States [1]
As S. aureus produce toxins that are extremely potent stimulators of T cells [4], we hypothesized that T cells may play a role in the early antimicrobial response to bacterial toxins by producing IL-26, which, in turn, inhibits bacterial growth and immune evasion
IL-26 mRNA was induced at staphylococcal enterotoxin-A (SEA) concentrations as low as 1-5 ng/ml, whereas optimal IL-26 induction was observed at a SEA concentration of 10 ng/ml (Figure 1A)
Summary
Staphylococcus aureus is a major cause of lifethreatening infections such as bacteremia, sepsis, and endocarditis and account for approximately 19,000 deaths per year in the United States [1]. We show that (i) skin T cells in chronic wounds infected with S. aureus express interleukin-26 (IL-26) in situ, (ii) staphylococcal enterotoxins (SE) trigger IL-26 expression in T cell lines and primary skin T cells, and (iii) IL-26 triggers death and inhibits biofilm formation and growth of S. aureus. Multiple host defense mechanisms against S. aureus have been identified including anti-microbial peptides, antibodies, neutrophils and IL-17 producing helper T (TH17) cells [9].
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