Publications by authors named "P M Schlievert"

Article Synopsis
  • Atopic dermatitis (AD) is an inflammatory skin condition linked to varying levels of Staphylococcus aureus, which affects disease severity and responds to treatments like dupilumab.
  • This study aimed to identify host genes related to S aureus levels and AD severity using data from a clinical trial involving 71 adults with moderate-to-severe AD.
  • The findings revealed a positive correlation between CERS1 expression (a gene associated with skin lipids) and both S aureus abundance and AD severity, suggesting CERS1 could serve as a biomarker for skin barrier dysfunction, with changes observable after dupilumab treatment.
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Background: Dedicator of cytokinesis 8 (DOCK8)-deficient patients have severe eczema, elevated IgE, and eosinophilia, features of atopic dermatitis (AD).

Objective: We sought to understand the mechanisms of eczema in DOCK8 deficiency.

Methods: Skin biopsy samples were characterized by histology, immunofluorescence microscopy, and gene expression.

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Glycerol Monolaurate (GML) is a naturally occurring fatty acid monoester with antimicrobial properties. is an agent of bioterrorism known for its unique lipopolysaccharide structure and low immunogenicity. Here we assessed whether exogenous GML would inhibit the growth of .

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Article Synopsis
  • A variety of diseases can be caused by a specific organism, including mild skin infections and severe conditions like pneumonia and sepsis.
  • The organism attacks mucosal and skin barriers, triggering harmful inflammation by promoting the release of chemokines from epithelial cells.
  • Researchers have cloned and characterized a new secreted protein that mainly functions to stimulate chemokine production, potentially aiding the organism in penetrating host defenses.
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Individuals with atopic dermatitis (AD) are highly colonized by and are more susceptible to severe viral complications. We hypothesized that secreted virulence factors may alter keratinocyte biology to enhance viral susceptibility through disruption of the skin barrier, impaired keratinocyte differentiation, and/or inflammation. To address this hypothesis, human keratinocytes were exposed to conditioned media from multiple strains that vary in virulence factor production (USA300, HG003, and RN4220) or select purified virulence factors.

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