Oleate Hydratase (OhyA) Is a Virulence Determinant in Staphylococcus aureus.

Staphylococcus aureus is an important pathogen that relies on a variety of mechanisms to evade and counteract the immune system. We show that S. aureus uses oleate hydratase (OhyA) to convert host -9 unsaturated fatty acids to their 10-hydroxy derivatives in human serum and at the infection site in a mouse neutropenic thigh model.

Host Fatty Acid Utilization by Staphylococcus aureus at the Infection Site.

utilizes the fatty acid (FA) kinase system to activate exogenous FAs for membrane synthesis. We developed a lipidomics workflow to determine the membrane phosphatidylglycerol (PG) molecular species synthesized by at the thigh infection site. Wild-type utilizes both host palmitate and oleate to acylate the 1 position of PG, and the 2 position is occupied by pentadecanoic acid arising from biosynthesis.

Oleate hydratase from protects against palmitoleic acid, the major antimicrobial fatty acid produced by mammalian skin.

Oleate hydratases (OhyAs) belong to a large family of bacterial proteins catalyzing the hydration or isomerization of double bonds in unsaturated fatty acids. A gene () is predicted to encode an OhyA. Here, we recombinantly expressed and purified OhyA and found that it forms a homodimer that requires FAD for activity.

MsaB and CodY Interact To Regulate Staphylococcus aureus Capsule in a Nutrient-Dependent Manner.

has a complex regulatory network for controlling the production of capsule polysaccharide. In , capsule production is controlled by several regulators in response to various environmental stimuli. Previously, we described MsaB as a new regulator that specifically binds to the promoter in a growth phase- or nutrient-dependent manner.

MsaB activates capsule production at the transcription level in Staphylococcus aureus.

Staphylococcus aureus produces several virulence factors that allow it to cause a variety of infections. One of the major virulence factors is the capsule, which contributes to the survival of the pathogen within the host as a way to escape phagocytosis. The production of the capsular polysaccharide is encoded in a 16 gene operon, which is regulated in response to several environmental stimuli including nutrient availability.

Molecular and phenotypic characterization of methicillin-resistant Staphylococcus aureus isolates causing bacteremia at a major hospital in southern Mississippi.

Staphylococcus aureus is the predominant cause of bacteremia worldwide. We assessed the molecular epidemiology and antibiotic resistance of methicillin-resistant S aureus isolates causing bacteremia in southern Mississippi. Diverse genetic backgrounds in terms of staphylococcal cassette chromosome mec, pulsed-field gel electrophoresis, and multilocus sequence typing types of methicillin-resistant S aureus were identified as causing bacteremia in Mississippi.

msaABCR operon positively regulates biofilm development by repressing proteases and autolysis in Staphylococcus aureus.

Staphylococcus aureus is an important human pathogen that causes nosocomial and community-acquired infections. One of the most important aspects of staphylococcal infections is biofilm development within the host, which renders the bacterium resistant to the host's immune response and antimicrobial agents. Biofilm development is very complex and involves several regulators that ensure cell survival on surfaces within the extracellular polymeric matrix.