Making the Most of the Host; Targeting the Autophagy Pathway Facilitates Intracellular Survival in Neutrophils.

The success of as a human commensal and an opportunistic pathogen relies on its ability to adapt to several niches within the host. The innate immune response plays a key role in protecting the host against infection; however, adeptness at evading the innate immune system is indisputably evident. The "Trojan horse" theory has been postulated to describe a mechanism by which takes advantage of phagocytes as a survival niche within the host to facilitate dissemination of to secondary sites during systemic infection.

Manipulation of Autophagy and Apoptosis Facilitates Intracellular Survival of in Human Neutrophils.

Polymorphonuclear neutrophils (PMN) are critical for first line innate immune defence against . Mature circulating PMN maintain a short half-life ending in constitutive apoptotic cell death. This makes them unlikely candidates as a bacterial intracellular niche.

Toll-like receptor 2-dependent endosomal signaling by in monocytes induces type I interferon and promotes intracellular survival.

Pathogen activation of innate immune pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) stimulates cellular signaling pathways. This often leads to outcomes that contribute to pathogen clearance. Alternatively, activation of specific PRR pathways can aid pathogen survival.

Clumping factor B is an important virulence factor during Staphylococcus aureus skin infection and a promising vaccine target.

Staphylococcus aureus expresses a number of cell wall-anchored proteins that mediate adhesion and invasion of host cells and tissues and promote immune evasion, consequently contributing to the virulence of this organism. The cell wall-anchored protein clumping factor B (ClfB) has previously been shown to facilitate S. aureus nasal colonization through high affinity interactions with the cornified envelope in the anterior nares.

IL-10 Plays Opposing Roles during Systemic and Localized Infections.

IL-10 is a potent anti-inflammatory mediator that plays a crucial role in limiting host immunopathology during bacterial infections by controlling effector T cell activation. has previously been shown to manipulate the IL-10 response as a mechanism of immune evasion during chronic systemic and biofilm models of infection. In the present study, we demonstrate divergent roles for IL-10 depending on the site of infection.

Staphylococcus aureus and Influenza A Virus: Partners in Coinfection.

Nasal carriage of Staphylococcus aureus is a significant risk factor for secondary staphylococcal pneumonia in influenza A virus (IAV)-infected hosts. However, little research has been undertaken to define the environmental and physiological changes that cause S. aureus to shift from commensal to pathogenic organism in this setting.

Host-Bacterial Crosstalk Determines Staphylococcus aureus Nasal Colonization.

Staphylococcus aureus persistently colonizes the anterior nares of approximately one fifth of the population and nasal carriage is a significant risk factor for infection. Recent advances have significantly refined our understanding of S. aureus-host communication during nasal colonization.

Nlrp-3-driven interleukin 17 production by γδT cells controls infection outcomes during Staphylococcus aureus surgical site infection.

Recent work has identified T cells and the cytokines they produce as important correlates of immune protection during Staphylococcus aureus infections through the ability of these T cells to regulate local neutrophil responses. However, the specific T-cell subsets that are involved in coordinating protection at distinct sites of infection remains to be established. In this study, we identify for the first time an important role for γδT cells in controlling S.

Nasal colonisation by Staphylococcus aureus depends upon clumping factor B binding to the squamous epithelial cell envelope protein loricrin.

Staphylococcus aureus asymptomatically colonises the anterior nares, but the host and bacterial factors that facilitate colonisation remain incompletely understood. The S. aureus surface protein ClfB has been shown to mediate adherence to squamous epithelial cells in vitro and to promote nasal colonisation in both mice and humans.