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Melissa officinalis extract selectively suppresses STAT1 signaling in oral epithelial cells
Issam Rasheed1,2, Layla Panahipour1, Ronald A Glabonjat3
1Department of Oral Biology, University Clinic of Dentistry, Medical University of Vienna, Vienna, Austria.
Abstract:
Oral inflammatory diseases such as oral lichen planus are characterized by dysregulated chemokine production and persistent interferon-associated signaling, with JAK/STAT pathways playing a central role in epithelial-immune crosstalk. Here, we investigated whether Melissa officinalis extract (MOE), a widely used phytomedicine with incompletely defined mechanisms, modulates inflammatory signaling in oral epithelial cells. MOE composition was characterized by HPLC-HRMS, and transcriptomic, RT-qPCR, ELISA, immunofluorescence, and cell-free kinase analyses were employed to define its biological effects in HSC2 and non-transformed epithelial cells. MOE was cytocompatible and selectively attenuated interferon-associated signaling rather than broadly suppressing inflammation. It markedly reduced interferon-stimulated gene expression, including MX1/2, IFIT and OAS family members, STAT1/2, CXCL10, and GBP1, while NF-κB-dependent CXCL8 expression remained unaffected. Mechanistically, MOE reduced JAK2 activity in a cell-free assay and suppressed STAT1 phosphorylation-associated nuclear translocation, supporting modulation of canonical interferon signaling. Consistently, MOE reduced CXCL10 expression at both mRNA and protein levels, and these effects occurred independently of reactive oxygen species modulation. Chemical profiling identified several phenolic acids, among which caffeic acid showed activity in suppressing CXCL10 production. These findings identify MOE as a pathway-selective modulator of interferon-driven inflammatory responses in oral epithelial cells, provide mechanistic insight into its clinical use, and support further investigation of Melissa officinalis-derived preparations as topical strategies for targeted modulation of mucosal inflammation.
Insights
Melissa officinalis extract (MOE) selectively targets interferon signaling in oral epithelial cells, reducing key inflammatory genes like CXCL10. This phytomedicine offers a targeted approach for mucosal inflammation, distinct from broad immunosuppression.
Area of Science:
- Oral biology
- Immunology
- Pharmacology
Background:
- Oral inflammatory diseases involve chemokine dysregulation and interferon signaling.
- Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathways are crucial in oral epithelial-immune interactions.
- The precise mechanisms of Melissa officinalis extract (MOE) in modulating oral inflammation are not fully understood.
Purpose of the Study:
- To investigate if Melissa officinalis extract (MOE) modulates inflammatory signaling pathways in oral epithelial cells.
- To elucidate the specific mechanisms by which MOE affects interferon-associated signaling.
- To characterize the chemical composition of MOE and identify active compounds.
Main Methods:
- High-performance liquid chromatography-high-resolution mass spectrometry (HPLC-HRMS) for MOE composition analysis.
- Transcriptomic, RT-qPCR, ELISA, and immunofluorescence assays to assess MOE's effects on gene and protein expression.
- Cell-free kinase assays to evaluate JAK2 activity and STAT1 phosphorylation.
Main Results:
- MOE demonstrated cytocompatibility and selectively reduced interferon-stimulated gene expression (e.g., MX1/2, IFIT, OAS, STAT1/2, CXCL10, GBP1).
- NF-κB-dependent CXCL8 expression was unaffected by MOE.
- MOE inhibited JAK2 activity and STAT1 phosphorylation-dependent nuclear translocation, confirming modulation of canonical interferon signaling.
- Caffeic acid, a phenolic acid in MOE, was identified as a potential active compound for CXCL10 suppression.
Conclusions:
- MOE acts as a pathway-selective modulator of interferon-driven inflammatory responses in oral epithelial cells.
- The findings provide mechanistic insights into MOE's clinical applications for oral inflammatory conditions.
- Melissa officinalis-derived preparations warrant further investigation as topical agents for targeted mucosal inflammation modulation.
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