This work was supported by the Roche Research Fund for Biology, the Bonizzi-Theler Stiftung, the GEBERT-RÜF-STIFTUNG, the Swiss National Science Foundation, the Vontobel Foundation, and UBS AG on behalf of a client. Conflict of interest: The authors declare no financial

or commercial conflict of interest. “
“Mast cells are proposed to be one of the targets for mucosal vaccine adjuvants. We previously demonstrated that mucosal adjuvants containing IgG immune complexes could activate connective tissue mast cells enhancing immune responses. Here we suggest that mucosal mast cells (MMC) may also contribute to augmentation of antigen-specific selleckchem immune responses following treatment with antigens complexed with IgG. We demonstrated that both bone marrow (BM)-derived cultured MMC and tissue resident MMC incorporated ovalbumin (OVA) at a greater level in the presence of anti-OVA IgG. Co-culture of OVA/IgG-pulsed BM-derived

MMC with splenocytes from OT-II mice promoted OVA-specific activation and proliferation of T cells, a process known as cross-presentation. Furthermore, BM-derived cultured MMC underwent apoptosis following treatment with IgG immune complexes, a feature that has been described to favour phagocytosis of mast cells by professional antigen-presenting cells. This article is protected by copyright. All rights reserved. “
“Infections caused Selleck Fostamatinib by the Racecadotril leading nosocomial pathogen Staphylococcus epidermidis are characterized by biofilm formation on implanted medical devices. In a previous study, we found that ClpP protease plays an essential role in biofilm formation of S. epidermidis. However, the mechanism by which ClpP impacts S. epidermidis biofilms has remained unknown. Here, we show that the Spx protein accumulates in the clpP mutant strain of S. epidermidis and controls biofilm formation of S. epidermidis via a pronounced effect on the transcription of the icaADBC operon coding

for the production of the biofilm exopolysaccharide polysaccharide intercellular adhesion (PIA). Notably, in contrast to Staphylococcus aureus, Spx controls PIA expression via an icaR-independent mechanism. Furthermore, Spx affected primary surface attachment, although not by regulating the production of the autolysin AtlE. Our results indicate that ClpP enhances the formation of S. epidermidis biofilms by degrading Spx, a negative regulator of biofilm formation. Staphylococcus epidermidis, previously regarded as an innocuous commensal bacterium of the human skin, has emerged as one of the most frequent causes of nosocomial infection in recent years. Staphylococcus epidermidis may cause persistent infections by forming biofilms on implanted medical devices, such as central venous catheters, urinary catheters, prosthetic heart valves and orthopedic devices.