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.
authors.affiliation: Department of Periodontology and Endodontology, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-18-15 Kuramoto, Tokushima 770-8504, Japan.
authors.forename: Yuka
authors.initials: Y
authors.lastname: Hiroshima
authors.forename: Mika
authors.initials: M
authors.lastname: Bando
authors.forename: Masatoshi
authors.initials: M
authors.lastname: Kataoka
authors.forename: Yuji
authors.initials: Y
authors.lastname: Inagaki
authors.forename: Mark C
authors.initials: MC
authors.lastname: Herzberg
authors.forename: Karen F
authors.initials: KF
authors.lastname: Ross
authors.forename: Kazuo
authors.initials: K
authors.lastname: Hosoi
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Nagata
authors.forename: Jun-Ichi
authors.initials: J
authors.lastname: Kido
mesh_terms: D000209:Acute-Phase Proteins / Q000032:analysis; D000293:Adolescent; D000328:Adult; D000890:Anti-Infective Agents / Q000276:immunology*; D023181:Antimicrobial Cationic Peptides / Q000276:immunology*; D015153:Blotting, Western; D040501:Calgranulin A / Q000032:analysis; D040502:Calgranulin B / Q000032:analysis; D018929:Cell Culture Techniques; D055316:Cystatin C / Q000032:analysis; D005260:Female; D005786:Gene Expression Regulation; D005881:Gingiva / Q000166:cytology / Q000276:immunology*; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology; D053582:Interleukin-1alpha / Q000276:immunology*; D015603:Keratinocytes / Q000276:immunology*; D000071068:Lipocalin-2; D054834:Lipocalins / Q000032:analysis; D008297:Male; D020411:Oligonucleotide Array Sequence Analysis; D055232:Proline-Rich Protein Domains / Q000276:immunology; D011518:Proto-Oncogene Proteins / Q000032:analysis; D000075023:S100 Calcium Binding Protein A7; D009418:S100 Proteins / Q000032:analysis; D000067616:S100A12 Protein; D053481:Secretory Leukocyte Peptidase Inhibitor / Q000032:analysis; D015842:Serine Proteinase Inhibitors / Q000032:analysis; D015854:Up-Regulation; D055815:Young Adult; D023083:beta-Defensins / Q000032:analysis / Q000276:immunology
chemical_list: D000209:Acute-Phase Proteins; D000890:Anti-Infective Agents; D023181:Antimicrobial Cationic Peptides; C525030:CST3 protein, human; D040501:Calgranulin A; D040502:Calgranulin B; D055316:Cystatin C; C106641:DEFB4A protein, human; D053582:Interleukin-1alpha; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D011518:Proto-Oncogene Proteins; D000075023:S100 Calcium Binding Protein A7; D009418:S100 Proteins; D000067616:S100A12 Protein; C090441:S100A12 protein, human; C089242:S100A7 protein, human; D053481:Secretory Leukocyte Peptidase Inhibitor; D015842:Serine Proteinase Inhibitors; D023083:beta-Defensins