In cystic fibrosis (CF) infectious and allergic airway inflammation cause pulmonary exacerbations that destroy the lungs. Staphylococcus aureus is a common long-term colonizer and cause of recurrent airway infections in CF. The pathogen is also associated with respiratory allergy; especially the staphylococcal serine protease-like proteins (Spls) can induce type 2 immune responses in humans and mice. We measured the serum IgE levels specific to 7 proteases of S. aureus by ELISA, targeting 5 Spls (76 CF patients and 46 controls) and the staphopains A and B (16 CF patients and 46 controls). Then we compared cytokine release and phenotype of T cells that had been stimulated with Spls between 5 CF patients and 5 controls. CF patients had strongly increased serum IgE binding to all Spls but not to the staphopains. Compared to healthy controls, their Spl-stimulated T cells released more type 2 cytokines (IL-4, IL-5, IL-13) and more IL-6 with no difference in the secretion of type 1- or type 3 cytokines (IFNγ, IL-17A, IL-17F). IL-10 production was low in CF T cells. The phenotype of the Spl-exposed T cells shifted towards a Th2 or Th17 profile in CF but to a Th1 profile in controls. Sensitization to S. aureus Spls is common in CF. This discovery could explain episodes of allergic inflammation of hitherto unknown causation in CF and extend the diagnostic and therapeutic portfolio.

Staphylococcus aureus bacteremia (SAB) is a frequent, severe condition that occurs in patients of all age groups and affects clinical departments of all medical fields. It is associated with a high mortality rate of 20–30%. In this study, we analyzed patient mortality associated with SAB at our tertiary care university hospital, assessed the clinical management in terms of administered antimicrobial therapy, and determined which factors have an impact on the clinical course and outcome of patients with this disease. We collected clinical data and blood culture isolates of 178 patients diagnosed with SAB between May 2013 and July 2015. For this study, bacteria were cultured and analyzed concerning their phenotype, hemolysis activity, biofilm formation, nuclease activity, prevalence of toxin genes, spa and agr type. Overall mortality was 24.2% and 30-day mortality was 14.6%. Inadequate initial therapy was administered to 26.2% of patients and was associated with decreased survival (p = 0.041). Other factors associated with poor survival were patient age (p = 0.003), agr type 4 (p ≤ 0.001) and pathological leukocyte counts (p = 0.029 if elevated and p = 0.003 if lowered). The type of infection focus, spa clonal complex and enterotoxin genes seg and sei had an impact on severity of inflammation. Our results indicate that mortality and burden of disease posed by SAB are high at our university hospital.