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Articles by Mohini Bhattacharya
Staphylococcus aureus biofilm extracellular DNA neutralizes the antimicrobial activity of histone H3
Abstract Staphylococcus aureus is an opportunistic pathogen that forms robust biofilms. This poses several challenges to the host in successfully clearing the pathogen, thus leading to chronic infections. S. aureus biofilms combat neutrophils by releasing pore-forming toxins called leukocidins. This leads to the induction of neutrophil extracellular traps (NETs) and neutrophil death. NETs are primarily composed of host DNA laced with several potent antimicrobials, including histones.
Skin androgens regulate Staphylococcus aureus pathogenicity via quorum sensing - Nature Microbiology Original
Abstract Skin cells secrete testosterone, with greater amounts secreted at the skin surface of males compared with females. Males are also more susceptible to skin infections than females. Here we report that mice engineered with testosterone-deficient skin are resistant to methicillin-resistant Staphylococcus aureus infections. Testosterone promoted the expression of S.
Matrix porosity is associated with Staphylococcus aureus biofilm survival during prosthetic joint infection
Abstract Biofilms are a cause of chronic, non-healing infections. Staphylococcus aureus is a proficient biofilm forming pathogen commonly isolated from prosthetic joint infections that develop following primary arthroplasty. Extracellular adhesion protein (Eap), previously characterized in planktonic or non-biofilm populations as being an adhesin and immune evasion factor, was recently identified in the exoproteome of S. aureus biofilms.
Polymicrobial interactions between Staphylococcus aureus and Pseudomonas aeruginosa promote biofilm formation and persistence in chronic wound infections
Abstract Chronic, non-healing wounds are a leading cause of prolonged patient morbidity and mortality, often due to biofilm- associated, polymicrobial infections. Staphylococcus aureus and Pseudomonas aeruginosa are the most frequently co-isolated pathogens from chronic wound infections. Competitive interactions between these pathogens contribute to enhanced virulence, persistence, and antimicrobial tolerance. P. aeruginosa utilizes the extracellular proteases LasB, LasA, and AprA to degrade S.
Collagen binding adhesin restricts Staphylococcus aureus skin infection
Abstract Staphylococcus aureus causes approximately 80% of skin and soft tissue infections (SSTIs). Collagen is the most abundant human extracellular matrix protein with critical roles in wound healing, and S. aureus encodes a collagen binding adhesin (Cna). The role of this protein during skin infections is unknown. Here we report that inability to bind collagen results in worsened pathology of intradermal δcna S. aureus infection. WT/Cna+ S.
Androgens at the skin surface regulate S. aureus pathogenesis through the activation of agr quorum sensing
Abstract Staphylococcus aureus, the most frequent cause of skin infections, is more common in men than women and selectively colonizes the skin during inflammation. Yet, the specific cues that drive infection in these settings remain unclear. Here we show that the host androgens testosterone and dihydrotestosterone promote S. aureus pathogenesis and skin infection. Without the secretion of these hormones, skin infection in vivo is limited. Testosterone activates S.
Breaking bad
DNASE1 (D1) and DNASE1L3 (D1L3) synergistically reduce the severity of systemic infections caused by Staphylococcus aureus. In this issue of JEM, Lacey et al. (2023. J. Exp. Med.https://doi.org/10.1084/jem.20221086) develop D1−/−, D1L3−/−, and D1−/−D1L3−/− mice to show that exogenous addition of the DNase formulation Dornase alfa can facilitate removal of biofilms.
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