aureus had lower anti-Map antibody titers than noncarriers. As an association of a chronic carrier status and the humoral anti-Eap response was not the goal of our study, we did not examine for a putative carrier status in our cohort, and therefore, in our study, an influence of carrier status cannot be excluded. Of note, in the study by Dryla and colleagues, serum sampling was performed at an early stage

of infection (2–8 days after the onset of disease), with the induction of IgG probably being not fully elicited, and in addition, an antigen was used that did not correspond to full-length Map/Eap (Hussain et al., 2008). Previous studies showed that antibodies against a number of antigens can confer a certain benefit against S. aureus diseases as demonstrated in animal models (Lee et al., 1997; McKenney et al., 1999). However, to date, most trials for a commercial utilization in

humans have failed to confirm clinical efficacy selleck chemical (Deresinski, 2006). Dissemination and invasion of tissue by S. aureus is mainly controlled by complement-mediated opsonization and phagocytosis (Cunnion et al., 2003) accountable for the higher risk of invasive infections in patients with deficiencies in neutrophil functions (Spickett, 2008). Using fluorescent microsphere beads as a surrogate parameter for staphylococci, we could show that, even in the absence of any opsonizing antibodies, the presence of Eap-stimulated phagocytosis by monocytes/macrophages as well as granulocytes. Although the addition of antibodies enhanced uptake moderately, Cabozantinib Selleckchem Temsirolimus most importantly, the level of anti-Eap antibodies did not correlate with the amount of phagocytosed beads. These data indicate that anti-Eap antibodies do not enhance phagocytosis. As patients with severe infections were found to harbor high levels of anti-Eap antibodies, it may therefore be suggested that these antibodies do not prevent invasive infections, but may rather result from such. On the other hand, certain effects of Eap investigated in mice led to the possibility of the use of this molecule for the prophylaxis and/or the treatment of disease such

as autoimmune disorders or cancer (Xie et al., 2006; Schneider et al., 2007; Wang et al., 2010). Our current observation, i.e. the presence of anti-Eap antibodies in every adult, but not in mice, now raises an aspect of caution as it has not yet been determined whether specific antibodies could interfere with these putatively beneficial effects for the host. The ubiquitous presence of anti-Eap antibodies in patients and healthy individuals, however, clearly underlines the pre-eminent role both of Eap and of anti-Eap antibodies in the human response against S. aureus. Our special thanks are due to all patients who consented to participate in this study. Furthermore, we would like to thank Karin Hilgert and Sandra Schmitz for excellent technical support.