Propionibacterium acnes Induces Autophagy in Keratinocytes: Involvement of Multiple Mechanisms

Klára Megyeri, L. Orosz, Szilvia Bolla, Lilla Erdei, Zsolt Rázga, György Seprényi, E. Urbán, Kornélia Szabó, L. Kemény

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Propionibacterium acnes is a dominant member of the cutaneous microbiota. Herein, we evaluate the effects of different P. acnes strains and propionic acid on autophagy in keratinocytes. Our results showed that P. acnes strain 889 altered the architecture of the mitochondrial network; elevated the levels of microtubule-associated protein 1 light chain 3B-II, Beclin-1, and phospho-5′-adenosine-monophosphate-activated protein kinase α; stimulated autophagic flux; facilitated intracellular redistribution of microtubule-associated protein 1 light chain 3B; increased average number of autophagosomes per cell; and enhanced development of acidic vesicular organelles in the HPV-KER cell line. Propionic acid increased the level of phospho-5′-adenosine-monophosphate-activated protein kinase α enhanced lipidation of microtubule-associated protein 1 light chain 3B, stimulated autophagic flux, and facilitated translocation of microtubule-associated protein 1 light chain 3B into autophagosomes in HPV-KER cells. P. acnes strains 889 and 6609 and heat-killed strain 889 also stimulated autophagosome formation in primary keratinocytes to varying degrees. These results indicate that cell wall components and secreted propionic acid metabolite of P. acnes evoke mitochondrial damage successively, thereby triggering 5′-adenosine-monophosphate-activated protein kinase-associated activation of autophagy, which in turn facilitates the removal of dysfunctional mitochondria and promotes survival of keratinocytes. Thus, we suggest that low-level colonization of hair follicles with noninvasive P. acnes strains, by triggering a local increase in autophagic activity, might exert a profound effect on several physiological processes responsible for the maintenance of skin tissue homeostasis.

Original languageEnglish
Pages (from-to)750-759
Number of pages10
JournalJournal of Investigative Dermatology
Volume138
Issue number4
DOIs
Publication statusPublished - Apr 1 2018

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Propionibacterium acnes
Autophagy
Keratinocytes
Microtubule-Associated Proteins
Adenosine Monophosphate
Protein Kinases
Light
Tissue homeostasis
Cells
Fluxes
Mitochondria
Physiological Phenomena
Skin
Metabolites
Hair Follicle
Microbiota
Cellular Structures
Organelles
Cell Wall
Chemical activation

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Dermatology
  • Cell Biology

Cite this

Propionibacterium acnes Induces Autophagy in Keratinocytes : Involvement of Multiple Mechanisms. / Megyeri, Klára; Orosz, L.; Bolla, Szilvia; Erdei, Lilla; Rázga, Zsolt; Seprényi, György; Urbán, E.; Szabó, Kornélia; Kemény, L.

In: Journal of Investigative Dermatology, Vol. 138, No. 4, 01.04.2018, p. 750-759.

Research output: Contribution to journalArticle

Megyeri, Klára ; Orosz, L. ; Bolla, Szilvia ; Erdei, Lilla ; Rázga, Zsolt ; Seprényi, György ; Urbán, E. ; Szabó, Kornélia ; Kemény, L. / Propionibacterium acnes Induces Autophagy in Keratinocytes : Involvement of Multiple Mechanisms. In: Journal of Investigative Dermatology. 2018 ; Vol. 138, No. 4. pp. 750-759.
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AB - Propionibacterium acnes is a dominant member of the cutaneous microbiota. Herein, we evaluate the effects of different P. acnes strains and propionic acid on autophagy in keratinocytes. Our results showed that P. acnes strain 889 altered the architecture of the mitochondrial network; elevated the levels of microtubule-associated protein 1 light chain 3B-II, Beclin-1, and phospho-5′-adenosine-monophosphate-activated protein kinase α; stimulated autophagic flux; facilitated intracellular redistribution of microtubule-associated protein 1 light chain 3B; increased average number of autophagosomes per cell; and enhanced development of acidic vesicular organelles in the HPV-KER cell line. Propionic acid increased the level of phospho-5′-adenosine-monophosphate-activated protein kinase α enhanced lipidation of microtubule-associated protein 1 light chain 3B, stimulated autophagic flux, and facilitated translocation of microtubule-associated protein 1 light chain 3B into autophagosomes in HPV-KER cells. P. acnes strains 889 and 6609 and heat-killed strain 889 also stimulated autophagosome formation in primary keratinocytes to varying degrees. These results indicate that cell wall components and secreted propionic acid metabolite of P. acnes evoke mitochondrial damage successively, thereby triggering 5′-adenosine-monophosphate-activated protein kinase-associated activation of autophagy, which in turn facilitates the removal of dysfunctional mitochondria and promotes survival of keratinocytes. Thus, we suggest that low-level colonization of hair follicles with noninvasive P. acnes strains, by triggering a local increase in autophagic activity, might exert a profound effect on several physiological processes responsible for the maintenance of skin tissue homeostasis.

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