Retinoids Enhance the Expression of Cathelicidin Antimicrobial Peptide during Reactive Dermal Adipogenesis
| Autor: | Marc C. Liggins, Ling-juan Zhang, Richard L. Gallo, Fengwu Li, Tatsuya Dokoshi |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Keratinocytes
Staphylococcus aureus medicine.medical_treatment Immunology Retinoic acid Tretinoin medicine.disease_cause Article Cell Line Cathelicidin Transcriptome Mice Retinoids chemistry.chemical_compound Cathelicidins 3T3-L1 Cells Adipocytes medicine Animals Immunology and Allergy Skin Adipogenesis Innate immune system Chemistry Cell Differentiation Dermis Fibroblasts Staphylococcal Infections Antimicrobial Cell culture Cancer research Antimicrobial Cationic Peptides |
| Zdroj: | J Immunol |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.1900520 |
| Popis: | A subset of dermal fibroblasts undergo rapid differentiation into adipocytes in response to infection and acutely produce the cathelicidin antimicrobial peptide gene Camp. Vitamin A and other retinoids inhibit adipogenesis yet can show benefit to skin disorders, such as cystic acne, that are exacerbated by bacteria. We observed that retinoids potently increase and sustain the expression of Camp in preadipocytes undergoing adipogenesis despite inhibition of markers of adipogenesis, such as Adipoq, Fabp4, and Rstn. Retinoids increase cathelicidin in both mouse and human preadipocytes, but this enhancement of antimicrobial peptide expression did not occur in keratinocytes or a sebocyte cell line. Preadipocytes undergoing adipogenesis more effectively inhibited growth of Staphylococcus aureus when exposed to retinoic acid. Whole transcriptome analysis identified hypoxia-inducible factor 1-α (HIF-1α) as a mechanism through which retinoids mediate this response. These observations uncouple the lipid accumulation element of adipogenesis from the innate immune response and uncover a mechanism, to our knowledge previously unsuspected, that may explain therapeutic benefits of retinoids in some skin disorders. |
| Databáze: | OpenAIRE |
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