Neutrophil-Mediated Phagocytosis of Staphylococcus aureus

Abstract

Initial elimination of invading Staphylococcus aureus from the body is mediated by professional phagocytes. The neutrophil is the major phagocyte of the innate immunity and plays a key role in the host defense against staphylococcal infections. Opsonization of the bacteria with immunoglobulins and complement factors enables efficient recognition by the neutrophil that subsequently leads to intracellular compartmentalization and killing. Here, we provide a review of the key processes evolved in neutrophil-mediated phagocytosis of S. aureus and briefly describe killing. As S. aureus is not helpless against the professional phagocytes, we will also highlight its immune evasion arsenal related to phagocytosis.

The Staphylococcus aureus AirSR Two-Component System Mediates Reactive Oxygen Species Resistance via Transcriptional Regulation of Staphyloxanthin Production

“…If oxygen were present in the phagosome, it, too, would promote AirSR-mediated upregulation of STX and antioxidant protection. In support of this suggestion, STX has been shown to be important for bacterial survival when S. aureus is cultured with neutrophils (2), and AirSR is important for survival in blood, where neutrophils constitute 50 to 60% of all leukocytes (22,38). Furthermore, genetic mutations or pharmacological inhibition of the NADPH oxidase pathway in neutrophils eliminated the requirement for STX by S. aureus in both assays (2).…”

Staphylococcus aureus PerR Is a Hypersensitive Hydrogen Peroxide Sensor using Iron-mediated Histidine Oxidation

“…In contrast, a significant oxidation of PerR SA is observed in aerobically grown E. coli without external H 2 O 2 treatment, indicating that endogenously produced H 2 O 2 is sufficient to oxidize PerR SA (Fig. 5A) (35,36). However, the perR null mutant S. aureus strain, which is more resistant to H 2 O 2 than the wild type by constitutive expression of H 2 O 2 defense enzymes, exhibits attenuated virulence in our C. elegans model of infection (Fig.…”

Fc-Gamma Receptor Polymorphisms Predispose Patients to Infectious Complications After Liver Transplantation

“…MAC resistance by GPC is thought to be related to this thick peptidoglycan layer that forms a physical barrier for C5b-9 components to target the membrane (43). In contrast, the variety of components in the GPC cell wall can be directly targeted by naturally occurring IgG in the human sera, resulting in ADCC-mediated recognition through FcgRs in addition to classical pathway complement activation (44 Since the association between FcgR SNPs and susceptibility to some severe autoimmune diseases has been previously reported (12), there is probably an association between genotype frequencies of the three genes and patient original diseases, such as autoimmune hepatitis, primary sclerosing cholangitis, and primary biliary cirrhosis. Unfortunately, the number of subjects in this study was not sufficient to demonstrate the significance of FcgR SNPs among each original disease (Table S6).…”