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New insights into acne pathogenesis: Propionibacterium acnes activates the inflammasome


Contassot, Emmanuel; French, Lars E (2014). New insights into acne pathogenesis: Propionibacterium acnes activates the inflammasome. Journal of Investigative Dermatology, 134(2):310-313.

Abstract

The precise contribution of the commensal bacterium Propionibacterium acnes (P. acnes) in the inflammatory response associated with acne vulgaris remains controversial. In this issue Qin et al. show that P. acnes induces robust IL-1β secretion in monocytic cells by triggering the activation of the NLRP3 inflammasome. In vivo, the encounter of P. acnes and macrophages in the peri-follicular dermis could locally result in the release of substantial amounts of IL-1β and therefore exacerbate inflammation. Such findings suggest that molecules targeting IL-1β and/or the NLRP3 inflammasome may constitute new treatment possibilities for acne vulgaris.

Abstract

The precise contribution of the commensal bacterium Propionibacterium acnes (P. acnes) in the inflammatory response associated with acne vulgaris remains controversial. In this issue Qin et al. show that P. acnes induces robust IL-1β secretion in monocytic cells by triggering the activation of the NLRP3 inflammasome. In vivo, the encounter of P. acnes and macrophages in the peri-follicular dermis could locally result in the release of substantial amounts of IL-1β and therefore exacerbate inflammation. Such findings suggest that molecules targeting IL-1β and/or the NLRP3 inflammasome may constitute new treatment possibilities for acne vulgaris.

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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Dermatology Clinic
Dewey Decimal Classification:610 Medicine & health
Scopus Subject Areas:Life Sciences > Biochemistry
Life Sciences > Molecular Biology
Health Sciences > Dermatology
Life Sciences > Cell Biology
Language:English
Date:February 2014
Deposited On:26 Feb 2015 12:38
Last Modified:26 Jan 2022 05:49
Publisher:Elsevier
ISSN:0022-202X
OA Status:Closed
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1038/jid.2013.505
PubMed ID:24424454
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