Isotretinoin suppresses key pro-inflammatory cytokines at transcriptional and systemic levels in acne vulgaris
ARCHIVES OF DERMATOLOGICAL RESEARCH, vol.318, no.1, 2026 (SCI-Expanded, Scopus)
- Publication Type: Article / Article
- Volume: 318 Issue: 1
- Publication Date: 2026
- Doi Number: 10.1007/s00403-026-04880-5
- Journal Name: ARCHIVES OF DERMATOLOGICAL RESEARCH
- Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, EMBASE, Academic Search Ultimate (EBSCO), Biomedical Reference Collection: Corporate Edition (EBSCO), Health Research Premium Collection (ProQuest), Pharma Collection (ProQuest)
- Istanbul University Affiliated: Yes
Abstract
Acne vulgaris (AV) is a chronic inflammatory disorder of the pilosebaceous unit in which pro-inflammatory cytokines contribute to lesion development and severity. Oral isotretinoin is an effective treatment for moderate-to-severe AV, but its systemic and transcriptional immunomodulatory effects remain incompletely characterized. This study aimed to investigate serum cytokine levels and expression profiles of selected pro-inflammatory markers in patients with AV before and after oral isotretinoin treatment. Fifty patients with moderate-to-severe AV receiving oral isotretinoin therapy and fifty healthy controls were enrolled. Serum levels of IL-1 alpha, IL-1 beta, TNF-alpha, IL-8 and IFN-gamma were quantified by multiplex ELISA, and peripheral blood leukocyte mRNA expression of the same targets was assessed by RT-qPCR. Paired pre/post comparisons, comparisons with healthy controls, and correlation analyses were performed. Serum levels of pro-inflammatory cytokines decreased after isotretinoin therapy, accompanied by reduced transcript levels of these mediators. Gene expression and serum concentrations were positively correlated for all evaluated cytokines. Change in acne severity (triangle IGA) was significantly associated with reduction in serum IL-1 beta levels, whereas the association with IL-8 did not remain significant after correction for multiple testing. Oral isotretinoin therapy was associated with coordinated suppression of key pro-inflammatory pathways at both transcript and protein levels. The association between clinical improvement and decreased IL-1 beta supports a potential role for the IL-1 beta axis in treatment-associated inflammatory change. These findings suggest that IL-1 beta may represent a potential biomarker of treatment-associated inflammatory modulation, although further validation is required.