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Int J Mol Sci. 2019 Jul 17;20(14). pii: E3510. doi: 10.3390/ijms20143510.

Suppression of Propionibacterium acnes-Induced Skin Inflammation by Laurus nobilis Extract and Its Major Constituent Eucalyptol.

Author information

1
Department of Molecular Bioscience, College of Biomedical Science, Institute of Bioscience & Biotechnology, Kangwon National University, Chuncheon 24341, Korea.
2
R&D Center, Greensolutions Co., Chuncheon 24342, Korea.
3
Department of Molecular Bioscience, College of Biomedical Science, Institute of Bioscience & Biotechnology, Kangwon National University, Chuncheon 24341, Korea. suryeonseo@kangwon.ac.kr.

Abstract

Acne is an inflammatory skin disorder in puberty with symptoms including papules, folliculitis, and nodules. Propionibacterium acnes (P. acnes) is the main anaerobic bacteria that cause acne. It is known to proliferate within sebum-blocked skin hair follicles. P. acnes activates monocytic cell immune responses to induce the expression of proinflammatory cytokines. Although the anti-inflammatory function of the Laurus nobilis (L. nobilis) extract (LNE) on several immunological disorders have been reported, the effect of LNE in P. acnes-mediated skin inflammation has not yet been explored. In the present study, we examined the ability of the LNE to modulate the P. acnes-induced inflammatory signaling pathway, and evaluated its mechanism. LNE significantly suppressed the expression of P. acnes-mediated proinflammatory cytokines, such as IL-1β, IL-6, and NLRP3. We also found that LNE inhibited the inflammatory transcription factor NF-κB in response to P. acnes. In addition, eucalyptol, which is the main constituent of LNE, consistently inhibited P. acnes-induced inflammatory signaling pathways. Moreover, LNE significantly ameliorated P. acnes-induced inflammation in a mouse model of acne. We suggest for the first time that LNE hold therapeutic value for the improvement of P. acnes-induced skin inflammation.

KEYWORDS:

Laurus nobilis L.; NF-κB; Propionibacterium acnes; eucalyptol; inflammation; proinflammatory cytokines

PMID:
31319552
DOI:
10.3390/ijms20143510
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