ArticleJCI insight2023
Type I IFNs link skin-associated dysbiotic commensal bacteria to pathogenic inflammation and angiogenesis in rosacea.
Article in JCI insight, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Omics-based decoding of molecular and metabolic crosstalk in the skin barrier ecosystem.Cell death and differentiation · 2026Review
- Complete genome sequence of Heyndrickxia oleronia EISK28 isolated from human facial skin.BMC genomic data · 2025Article
- LAPTM5 exacerbates STING-mediated inflammation induced by LL-37 through stabilizing STING in rosacea.Communications biology · 2025Article
- Article
- Integrative Analysis of Fungal and Bacterial Microbiomes Across Skin, Blood, and Stool in Rosacea Patients.International journal of molecular sciences · 2025Article
- Microbiome-Based Products: Therapeutic Potential for Inflammatory Skin Diseases.International journal of molecular sciences · 2025Review
- Keratin 6A promotes skin inflammation through JAK1-STAT3 activation in keratinocytes.Journal of biomedical science · 2025Article
- Genetic association between human skin microbiota with vaginitis: a two-sample Mendelian randomization study.Archives of dermatological research · 2025Article
- Relationship of the Specific Inflammatory Cytokines KLK5, IL-8, and IL-22 withJournal of inflammation research · 2025Article
- Current Trends and Future Insights on Rosacea Treatment: A Bibliometric Analysis.Clinical, cosmetic and investigational dermatology · 2025Article
- Single-cell transcriptomics reveals aberrant skin-resident cell populations and identifies fibroblasts as a determinant in rosacea.Nature communications · 2024Article
- The role of plasmacytoid dendritic cells (pDCs) in immunity during viral infections and beyond.Cellular & molecular immunology · 2024Review
- High-sensitive sensory neurons exacerbate rosacea-like dermatitis in mice by activating γδ T cells directly.Nature communications · 2024Article
- IL-22 in Atopic Dermatitis.Cells · 2024Review
- The Gut and Skin Microbiome and Its Association with Aging Clocks.International journal of molecular sciences · 2024Review
- Elevated Specific Pro-Inflammatory Cytokines in Peripheral Circulation Indicate an Increased Risk of Anxiety and Depression in Rosacea.Journal of inflammation research · 2024Article
- Signaling pathways and targeted therapy for rosacea.Frontiers in immunology · 2024Review
- Therapeutic strategies focusing on immune dysregulation and neuroinflammation in rosacea.Frontiers in immunology · 2024Review
- The Notch signaling-regulated angiogenesis in rheumatoid arthritis: pathogenic mechanisms and therapeutic potentials.Frontiers in immunology · 2023Review
- Rosacea, microbiome and probiotics: the gut-skin axis.Frontiers in microbiology · 2023Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rosacea is a common chronic inflammatory skin disease with a fluctuating course of excessive inflammation and apparent neovascularization. Microbial dysbiosis with a high density of Bacillus oleronius and increased activity of kallikrein 5, which cleaves cathelicidin antimicrobial peptide, are key pathogenic triggers in rosacea. However, how these events are linked to the disease remains unknown. Here, we show that type I IFNs produced by plasmacytoid DCs represent the pivotal link between dysbiosis, the aberrant immune response, and neovascularization. Compared with other commensal bacteria, B. oleronius is highly susceptible and preferentially killed by cathelicidin antimicrobial peptides, leading to enhanced generation of complexes with bacterial DNA. These bacterial DNA complexes but not DNA complexes derived from host cells are required for cathelicidin-induced activation of plasmacytoid DCs and type I IFN production. Moreover, kallikrein 5 cleaves cathelicidin into peptides with heightened DNA binding and type I IFN-inducing capacities. In turn, excessive type I IFN expression drives neoangiogenesis via IL-22 induction and upregulation of the IL-22 receptor on endothelial cells. These findings unravel a potentially novel pathomechanism that directly links hallmarks of rosacea to the killing of dysbiotic commensal bacteria with induction of a pathogenic type I IFN-driven and IL-22-mediated angiogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.