Regulation of antimicrobial peptide expression in human gingival keratinocytes by interleukin-1α

Yuka Hiroshima; Mika Bando; Masatoshi Kataoka; Yuji Inagaki; Mark C. Herzberg; Karen F. Ross; Kazuo Hosoi; Toshihiko Nagata; Jun Ichi Kido

doi:10.1016/j.archoralbio.2011.01.004

Regulation of antimicrobial peptide expression in human gingival keratinocytes by interleukin-1α

Yuka Hiroshima, Mika Bando, Masatoshi Kataoka, Yuji Inagaki, Mark C. Herzberg, Karen F. Ross, Kazuo Hosoi, Toshihiko Nagata, Jun Ichi Kido

Diagnostic and Biological Sciences

Research output: Contribution to journal › Article › peer-review

38 Scopus citations

Abstract

In the oral cavity, mucosal keratinocytes resist bacterial infection, in part, by producing broad-spectrum antimicrobial peptides (AMPs) including defensin, adrenomedullin and calprotectin. Epidermal keratinocyte expression of many AMPs increases in response to interleukin-1α (IL-1α). IL-1α is produced by epidermal keratinocytes and regulates cell differentiation. To better understand innate immunity in the oral cavity, we sought to determine how IL-1α might regulate expression of AMPs by human gingival keratinocytes (HGKs) using DNA microarray and Western blot analyses. HGKs from three subjects expressed eleven AMPs, including S100A7, S100A8, S100A9, S100A12, secretory leucocyte protease inhibitor, lipocalin 2 (LCN2), cystatin C and β-defensin 2. Of the expressed AMPs, S100A7, S100A12 and LCN2 were up-regulated by IL-1α (inducible AMPs); the other AMPs were considered to be constitutive. Human gingival keratinocytes, therefore, express constitutive and IL-1α-inducible AMPs to provide a rapid and robust innate response to microbial infection.

Original language	English (US)
Pages (from-to)	761-767
Number of pages	7
Journal	Archives of Oral Biology
Volume	56
Issue number	8
DOIs	https://doi.org/10.1016/j.archoralbio.2011.01.004
State	Published - Aug 2011

Bibliographical note

Funding Information:
The authors are very grateful to Dr. Masaru Nagayama, Dr. Youji Miyamoto and Dr. Kazuhito Satomura (The University of Tokushima Graduate School) for the help to supply of gingival fragments. This study was supported in part by Grants-in Aid (19592388 and 21592625) for Scientific Research from the Japan Society for the Promotion and by NIH grants RO1DE11831 and RO1DE15503 to MCH.

Funding Information:
This study was supported in part by Grants-in Aid (19592388 and 21592625) for Scientific Research from the Japan Society for the Promotion and by NIH grants RO1DE11831 and RO1DE15503 to MCH.

Keywords

Antimicrobial peptide
Gingival keratinocyte
Interleukin-1α
Microarray analysis

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title = "Regulation of antimicrobial peptide expression in human gingival keratinocytes by interleukin-1α",

abstract = "In the oral cavity, mucosal keratinocytes resist bacterial infection, in part, by producing broad-spectrum antimicrobial peptides (AMPs) including defensin, adrenomedullin and calprotectin. Epidermal keratinocyte expression of many AMPs increases in response to interleukin-1α (IL-1α). IL-1α is produced by epidermal keratinocytes and regulates cell differentiation. To better understand innate immunity in the oral cavity, we sought to determine how IL-1α might regulate expression of AMPs by human gingival keratinocytes (HGKs) using DNA microarray and Western blot analyses. HGKs from three subjects expressed eleven AMPs, including S100A7, S100A8, S100A9, S100A12, secretory leucocyte protease inhibitor, lipocalin 2 (LCN2), cystatin C and β-defensin 2. Of the expressed AMPs, S100A7, S100A12 and LCN2 were up-regulated by IL-1α (inducible AMPs); the other AMPs were considered to be constitutive. Human gingival keratinocytes, therefore, express constitutive and IL-1α-inducible AMPs to provide a rapid and robust innate response to microbial infection.",

keywords = "Antimicrobial peptide, Gingival keratinocyte, Interleukin-1α, Microarray analysis",

author = "Yuka Hiroshima and Mika Bando and Masatoshi Kataoka and Yuji Inagaki and Herzberg, {Mark C.} and Ross, {Karen F.} and Kazuo Hosoi and Toshihiko Nagata and Kido, {Jun Ichi}",

note = "Funding Information: The authors are very grateful to Dr. Masaru Nagayama, Dr. Youji Miyamoto and Dr. Kazuhito Satomura (The University of Tokushima Graduate School) for the help to supply of gingival fragments. This study was supported in part by Grants-in Aid (19592388 and 21592625) for Scientific Research from the Japan Society for the Promotion and by NIH grants RO1DE11831 and RO1DE15503 to MCH. Funding Information: This study was supported in part by Grants-in Aid (19592388 and 21592625) for Scientific Research from the Japan Society for the Promotion and by NIH grants RO1DE11831 and RO1DE15503 to MCH. ",

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AU - Bando, Mika

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AU - Herzberg, Mark C.

AU - Ross, Karen F.

AU - Hosoi, Kazuo

AU - Nagata, Toshihiko

AU - Kido, Jun Ichi

N1 - Funding Information: The authors are very grateful to Dr. Masaru Nagayama, Dr. Youji Miyamoto and Dr. Kazuhito Satomura (The University of Tokushima Graduate School) for the help to supply of gingival fragments. This study was supported in part by Grants-in Aid (19592388 and 21592625) for Scientific Research from the Japan Society for the Promotion and by NIH grants RO1DE11831 and RO1DE15503 to MCH. Funding Information: This study was supported in part by Grants-in Aid (19592388 and 21592625) for Scientific Research from the Japan Society for the Promotion and by NIH grants RO1DE11831 and RO1DE15503 to MCH.

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N2 - In the oral cavity, mucosal keratinocytes resist bacterial infection, in part, by producing broad-spectrum antimicrobial peptides (AMPs) including defensin, adrenomedullin and calprotectin. Epidermal keratinocyte expression of many AMPs increases in response to interleukin-1α (IL-1α). IL-1α is produced by epidermal keratinocytes and regulates cell differentiation. To better understand innate immunity in the oral cavity, we sought to determine how IL-1α might regulate expression of AMPs by human gingival keratinocytes (HGKs) using DNA microarray and Western blot analyses. HGKs from three subjects expressed eleven AMPs, including S100A7, S100A8, S100A9, S100A12, secretory leucocyte protease inhibitor, lipocalin 2 (LCN2), cystatin C and β-defensin 2. Of the expressed AMPs, S100A7, S100A12 and LCN2 were up-regulated by IL-1α (inducible AMPs); the other AMPs were considered to be constitutive. Human gingival keratinocytes, therefore, express constitutive and IL-1α-inducible AMPs to provide a rapid and robust innate response to microbial infection.

AB - In the oral cavity, mucosal keratinocytes resist bacterial infection, in part, by producing broad-spectrum antimicrobial peptides (AMPs) including defensin, adrenomedullin and calprotectin. Epidermal keratinocyte expression of many AMPs increases in response to interleukin-1α (IL-1α). IL-1α is produced by epidermal keratinocytes and regulates cell differentiation. To better understand innate immunity in the oral cavity, we sought to determine how IL-1α might regulate expression of AMPs by human gingival keratinocytes (HGKs) using DNA microarray and Western blot analyses. HGKs from three subjects expressed eleven AMPs, including S100A7, S100A8, S100A9, S100A12, secretory leucocyte protease inhibitor, lipocalin 2 (LCN2), cystatin C and β-defensin 2. Of the expressed AMPs, S100A7, S100A12 and LCN2 were up-regulated by IL-1α (inducible AMPs); the other AMPs were considered to be constitutive. Human gingival keratinocytes, therefore, express constitutive and IL-1α-inducible AMPs to provide a rapid and robust innate response to microbial infection.

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Regulation of antimicrobial peptide expression in human gingival keratinocytes by interleukin-1α

Abstract

Bibliographical note

Keywords

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