Berberine Inhibits the Inflammatory Response Induced by Staphylococcus aureus Isolated from Atopic Eczema Patients via the TNF-α/Inflammation/RAGE Pathways
Atopic eczema patients exhibit high levels of ( ) skin colonization. can stimulate macrophages and the expression of proinflammatory cytokines. Berberine (BBR), an alkaloid, attenuates toxin production. This study investigated if BBR suppressed bacterial growth and inflammatory response induced by e...
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Veröffentlicht in: | Cells (Basel, Switzerland) Switzerland), 2024-10, Vol.13 (19), p.1639 |
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Hauptverfasser: | , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Atopic eczema patients exhibit high levels of
(
) skin colonization.
can stimulate macrophages and the expression of proinflammatory cytokines. Berberine (BBR), an alkaloid, attenuates
toxin production. This study investigated if BBR suppressed bacterial growth and inflammatory response induced by eczema-patient-derived
using murine macrophage (RAW 264.7) and human monocyte cell lines (U937). RAW 264.7 and U937 were treated with BBR at different concentrations and stimulated with heat-killed
(ATCC #33591) or
derived from severe eczema patients (EC01-EC10), who were undergoing topical steroid withdrawal, for 24 h. TNF-α protein levels were determined by ELISA, gene expression by qRT-PCR, cell cytotoxicity by trypan blue excursion, and reactive oxygen species (ROS) levels by fluorometric assay. BBR showed a bacteriostatic effect in
(ATCC strain #33591 and clinical isolates (EC01-EC10) and suppressed TNF-α production in RAW 264.7 and U937 cells exposed to heat-killed
(ATCC and clinical isolates) dose-dependently without any cell cytotoxicity. BBR (20 µg/mL) suppressed >90% of TNF-α production (
< 0.001), downregulated genes involved in inflammatory pathways, and inhibited
ROS production in U937 and RAW 264.7 cells (
< 0.01). BBR suppresses
-induced inflammation via inhibition of TNF-α release, ROS production, and expression of key genes involved in the inflammatory pathway. |
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ISSN: | 2073-4409 2073-4409 |
DOI: | 10.3390/cells13191639 |