G2A attenuates Propionibacterium acnes induction of inflammatory cytokines in human monocytes

Andrew J. Park, George W. Agak, Min Qin, Lisa D. Hisaw, Aslan Pirouz, Stephanie Kao, Laura J. Marinelli, Hermes J. Garbán, Diane Thiboutot, Philip T. Liu, Jenny Kim

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Background: Acne vulgaris is a disease of the pilosebaceous unit characterized by increased sebum production, hyperkeratinization, and immune responses to Propionibacterium acnes (PA). Here, we explore a possible mechanism by which a lipid receptor, G2A, regulates immune responses to a commensal bacterium. Objective: To elucidate the inflammatory properties of G2A in monocytes in response to PA stimulation. Furthermore, our study sought to investigate pathways by which lipids modulate immune responses in response to PA. Methods: Our studies focused on monocytes collected from human peripheral blood mononuclear cells, the monocytic cell line THP-1, and a lab strain of PA. Our studies involved the use of enzyme-linked immunosorbent, Western blot, reverse transcription polymerase chain reaction, small interfering RNA (siRNA), and microarray analysis of human acne lesions in the measurements of inflammatory markers. Results: G2A gene expression is higher in acne lesions compared to normal skin and is inducible by the acne therapeutic, 13-cis-retinoic acid. In vitro, PA induces both the Toll-like receptor 2-dependent expression of G2A as well as the production of the G2A ligand, 9-hydroxyoctadecadienoic acid, from human monocytes. G2A gene knockdown through siRNA enhances PA stimulation of interleukin (IL)-6, IL-8, and IL-1β possibly through increased activation of the ERK1/2 MAP kinase and nuclear factor kappa B p65 pathways. Conclusion: G2A may play a role in quelling inflammatory cytokine response to PA, revealing G2A as a potential attenuator of inflammatory response in a disease associated with a commensal bacterium.

Original languageEnglish (US)
Pages (from-to)688-698
Number of pages11
JournalAnnals of Dermatology
Volume29
Issue number6
DOIs
StatePublished - Dec 1 2017

Fingerprint

Propionibacterium acnes
Monocytes
Cytokines
Acne Vulgaris
Small Interfering RNA
Sebum
Gene Knockdown Techniques
Bacteria
Lipids
Toll-Like Receptor 2
Isotretinoin
Immunosorbents
Microarray Analysis
Interleukin-8
Interleukin-1
Reverse Transcription
Interleukin-6
Blood Cells
Western Blotting
Ligands

All Science Journal Classification (ASJC) codes

  • Dermatology

Cite this

Park, A. J., Agak, G. W., Qin, M., Hisaw, L. D., Pirouz, A., Kao, S., ... Kim, J. (2017). G2A attenuates Propionibacterium acnes induction of inflammatory cytokines in human monocytes. Annals of Dermatology, 29(6), 688-698. https://doi.org/10.5021/ad.2017.29.6.688
Park, Andrew J. ; Agak, George W. ; Qin, Min ; Hisaw, Lisa D. ; Pirouz, Aslan ; Kao, Stephanie ; Marinelli, Laura J. ; Garbán, Hermes J. ; Thiboutot, Diane ; Liu, Philip T. ; Kim, Jenny. / G2A attenuates Propionibacterium acnes induction of inflammatory cytokines in human monocytes. In: Annals of Dermatology. 2017 ; Vol. 29, No. 6. pp. 688-698.
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abstract = "Background: Acne vulgaris is a disease of the pilosebaceous unit characterized by increased sebum production, hyperkeratinization, and immune responses to Propionibacterium acnes (PA). Here, we explore a possible mechanism by which a lipid receptor, G2A, regulates immune responses to a commensal bacterium. Objective: To elucidate the inflammatory properties of G2A in monocytes in response to PA stimulation. Furthermore, our study sought to investigate pathways by which lipids modulate immune responses in response to PA. Methods: Our studies focused on monocytes collected from human peripheral blood mononuclear cells, the monocytic cell line THP-1, and a lab strain of PA. Our studies involved the use of enzyme-linked immunosorbent, Western blot, reverse transcription polymerase chain reaction, small interfering RNA (siRNA), and microarray analysis of human acne lesions in the measurements of inflammatory markers. Results: G2A gene expression is higher in acne lesions compared to normal skin and is inducible by the acne therapeutic, 13-cis-retinoic acid. In vitro, PA induces both the Toll-like receptor 2-dependent expression of G2A as well as the production of the G2A ligand, 9-hydroxyoctadecadienoic acid, from human monocytes. G2A gene knockdown through siRNA enhances PA stimulation of interleukin (IL)-6, IL-8, and IL-1β possibly through increased activation of the ERK1/2 MAP kinase and nuclear factor kappa B p65 pathways. Conclusion: G2A may play a role in quelling inflammatory cytokine response to PA, revealing G2A as a potential attenuator of inflammatory response in a disease associated with a commensal bacterium.",
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Park, AJ, Agak, GW, Qin, M, Hisaw, LD, Pirouz, A, Kao, S, Marinelli, LJ, Garbán, HJ, Thiboutot, D, Liu, PT & Kim, J 2017, 'G2A attenuates Propionibacterium acnes induction of inflammatory cytokines in human monocytes', Annals of Dermatology, vol. 29, no. 6, pp. 688-698. https://doi.org/10.5021/ad.2017.29.6.688

G2A attenuates Propionibacterium acnes induction of inflammatory cytokines in human monocytes. / Park, Andrew J.; Agak, George W.; Qin, Min; Hisaw, Lisa D.; Pirouz, Aslan; Kao, Stephanie; Marinelli, Laura J.; Garbán, Hermes J.; Thiboutot, Diane; Liu, Philip T.; Kim, Jenny.

In: Annals of Dermatology, Vol. 29, No. 6, 01.12.2017, p. 688-698.

Research output: Contribution to journalArticle

TY - JOUR

T1 - G2A attenuates Propionibacterium acnes induction of inflammatory cytokines in human monocytes

AU - Park, Andrew J.

AU - Agak, George W.

AU - Qin, Min

AU - Hisaw, Lisa D.

AU - Pirouz, Aslan

AU - Kao, Stephanie

AU - Marinelli, Laura J.

AU - Garbán, Hermes J.

AU - Thiboutot, Diane

AU - Liu, Philip T.

AU - Kim, Jenny

PY - 2017/12/1

Y1 - 2017/12/1

N2 - Background: Acne vulgaris is a disease of the pilosebaceous unit characterized by increased sebum production, hyperkeratinization, and immune responses to Propionibacterium acnes (PA). Here, we explore a possible mechanism by which a lipid receptor, G2A, regulates immune responses to a commensal bacterium. Objective: To elucidate the inflammatory properties of G2A in monocytes in response to PA stimulation. Furthermore, our study sought to investigate pathways by which lipids modulate immune responses in response to PA. Methods: Our studies focused on monocytes collected from human peripheral blood mononuclear cells, the monocytic cell line THP-1, and a lab strain of PA. Our studies involved the use of enzyme-linked immunosorbent, Western blot, reverse transcription polymerase chain reaction, small interfering RNA (siRNA), and microarray analysis of human acne lesions in the measurements of inflammatory markers. Results: G2A gene expression is higher in acne lesions compared to normal skin and is inducible by the acne therapeutic, 13-cis-retinoic acid. In vitro, PA induces both the Toll-like receptor 2-dependent expression of G2A as well as the production of the G2A ligand, 9-hydroxyoctadecadienoic acid, from human monocytes. G2A gene knockdown through siRNA enhances PA stimulation of interleukin (IL)-6, IL-8, and IL-1β possibly through increased activation of the ERK1/2 MAP kinase and nuclear factor kappa B p65 pathways. Conclusion: G2A may play a role in quelling inflammatory cytokine response to PA, revealing G2A as a potential attenuator of inflammatory response in a disease associated with a commensal bacterium.

AB - Background: Acne vulgaris is a disease of the pilosebaceous unit characterized by increased sebum production, hyperkeratinization, and immune responses to Propionibacterium acnes (PA). Here, we explore a possible mechanism by which a lipid receptor, G2A, regulates immune responses to a commensal bacterium. Objective: To elucidate the inflammatory properties of G2A in monocytes in response to PA stimulation. Furthermore, our study sought to investigate pathways by which lipids modulate immune responses in response to PA. Methods: Our studies focused on monocytes collected from human peripheral blood mononuclear cells, the monocytic cell line THP-1, and a lab strain of PA. Our studies involved the use of enzyme-linked immunosorbent, Western blot, reverse transcription polymerase chain reaction, small interfering RNA (siRNA), and microarray analysis of human acne lesions in the measurements of inflammatory markers. Results: G2A gene expression is higher in acne lesions compared to normal skin and is inducible by the acne therapeutic, 13-cis-retinoic acid. In vitro, PA induces both the Toll-like receptor 2-dependent expression of G2A as well as the production of the G2A ligand, 9-hydroxyoctadecadienoic acid, from human monocytes. G2A gene knockdown through siRNA enhances PA stimulation of interleukin (IL)-6, IL-8, and IL-1β possibly through increased activation of the ERK1/2 MAP kinase and nuclear factor kappa B p65 pathways. Conclusion: G2A may play a role in quelling inflammatory cytokine response to PA, revealing G2A as a potential attenuator of inflammatory response in a disease associated with a commensal bacterium.

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