International journal of dermatology · 2025
The Effect of Myrtacine and Celastrol-Enriched Extract on Cutibacterium acnes Extracellular Vesicles.
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Cheung Caroline T, Mias Céline, Lancien Ugo, Corvec Stéphane, Mengeaud Valérie, Khammari Amir, Duplan Hélène, Dréno Brigitte
Аннотация
BACKGROUND: Commensal bacteria interact with each other and their environment, secreting anti-microbial peptides, bacteriocins, and extracellular vesicles (EVs). Cutibacterium acnes (C. acnes), a commensal bacterium that plays a major role in acne, is classified into different phylotypes (IA1, IA2, IB, IC, II, and III), where overabundance of phylotype IA1 relative to other phylotypes is found in acne lesions. EVs secreted by C. acnes phylotype IA1 extracted from an acne lesion were previously found to induce a pro-inflammatory response in skin models. Here, we investigated the effects of Myrtus communis extract (Myrtacine) and Celastrol-enriched extract (CEE), anti-inflammatory ingredients, alone or in combination, on cutaneous innate immunity induced by C. acnes IA1 EVs.
METHODS: This study was conducted under preventive and modulating conditions: Myrtacine alone, CEE alone, or in combination were added to the culture medium either prior to (preventive) or after (modulating) incubation with C. acnes IA1 EVs from healthy and acne skin in immortalized keratinocytes (HaCaT) and human skin explants. Then, regulation of β-defensin 2 (hBD2), interleukin (IL)-6, IL-8, IL-17α, and IL-36ɣ was assessed.
RESULTS: Preventive and modulating applications of Myrtacine and CEE significantly reduced expression of the five immune markers induced specifically by EVs from acne-derived C. acnes IA1.
CONCLUSION: Our results show that C. acnes EVs may be a target of Myrtacine and CEE. They can down-modulate the pro-inflammatory activity induced by EVs derived from C. acnes IA1 from acne skin, showing the interest of these ingredients at both preventive and modulating levels in the treatment of inflammatory acne.
METHODS: This study was conducted under preventive and modulating conditions: Myrtacine alone, CEE alone, or in combination were added to the culture medium either prior to (preventive) or after (modulating) incubation with C. acnes IA1 EVs from healthy and acne skin in immortalized keratinocytes (HaCaT) and human skin explants. Then, regulation of β-defensin 2 (hBD2), interleukin (IL)-6, IL-8, IL-17α, and IL-36ɣ was assessed.
RESULTS: Preventive and modulating applications of Myrtacine and CEE significantly reduced expression of the five immune markers induced specifically by EVs from acne-derived C. acnes IA1.
CONCLUSION: Our results show that C. acnes EVs may be a target of Myrtacine and CEE. They can down-modulate the pro-inflammatory activity induced by EVs derived from C. acnes IA1 from acne skin, showing the interest of these ingredients at both preventive and modulating levels in the treatment of inflammatory acne.