Human β-defensin 2 is induced by interleukin-1β in the corneal epithelial cells

Jun Seop Shin, Chan Wha Kim, Young Sam Kwon, Jae Chan Kim

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Mammalian epithelia produce the various antimicrobial peptides against the bacterial or viral infection, thereby acting as the active immune modulators in the innate immunity. In this study, we examined the effects of the various proinflammatory cytokines or LPS on cell viability and antimicrobial β-defensin gene expressions in human corneal epithelial cells. Results showed that the cytokines or LPS did not exert severe cytotoxic effects on the cells, and that β-defensin 1 was constitutively expressed, while β-defensin 2 was specifically induced by IL-1β, supporting the idea that these cytokines or LPS involve the defense mechanism in the cornea. Furthermore, the reporter and gel shift assay to define the induction mechanism of β-defensin 2 by IL-1β demonstrated that the most proximal NF-κB site on the promoter region of β-defensin 2 was not critical for the process. Data obtained from the normal or patients with the varying ocular diseases showed that our in vitro results were relevant in the clinical settings. Our results clearly demonstrated that β-defensin 1 and 2 are important antimicrobial peptides in the corneal tissues, and that the mechanistic induction process of β-defensin 2 by IL-1β is not solely dependent on proximal NF-κB site activation, thus suggesting that the long distal portion of the promoter is needed for the full responsiveness toward IL-1β.

Original languageEnglish
Pages (from-to)204-210
Number of pages7
JournalExperimental and Molecular Medicine
Volume36
Issue number3
Publication statusPublished - 2004 Jun 30

Fingerprint

Defensins
Interleukin-1
Epithelial Cells
Cytokines
Peptides
Eye Diseases
Virus Diseases
Bacterial Infections
Innate Immunity
Genetic Promoter Regions
Gene expression
Cornea
Modulators
Assays
Cell Survival
Epithelium
Gels
Chemical activation
Cells
Tissue

Keywords

  • βdefensins
  • Antimicrobial cationic peptides
  • Cornea
  • Corneal epithelium
  • Gene expression regulation
  • Interleukin-1β

ASJC Scopus subject areas

  • Biochemistry
  • Genetics

Cite this

Human β-defensin 2 is induced by interleukin-1β in the corneal epithelial cells. / Shin, Jun Seop; Kim, Chan Wha; Kwon, Young Sam; Kim, Jae Chan.

In: Experimental and Molecular Medicine, Vol. 36, No. 3, 30.06.2004, p. 204-210.

Research output: Contribution to journalArticle

Shin, Jun Seop ; Kim, Chan Wha ; Kwon, Young Sam ; Kim, Jae Chan. / Human β-defensin 2 is induced by interleukin-1β in the corneal epithelial cells. In: Experimental and Molecular Medicine. 2004 ; Vol. 36, No. 3. pp. 204-210.
@article{373fb852854c4c4f8182c7b88a98a1f1,
title = "Human β-defensin 2 is induced by interleukin-1β in the corneal epithelial cells",
abstract = "Mammalian epithelia produce the various antimicrobial peptides against the bacterial or viral infection, thereby acting as the active immune modulators in the innate immunity. In this study, we examined the effects of the various proinflammatory cytokines or LPS on cell viability and antimicrobial β-defensin gene expressions in human corneal epithelial cells. Results showed that the cytokines or LPS did not exert severe cytotoxic effects on the cells, and that β-defensin 1 was constitutively expressed, while β-defensin 2 was specifically induced by IL-1β, supporting the idea that these cytokines or LPS involve the defense mechanism in the cornea. Furthermore, the reporter and gel shift assay to define the induction mechanism of β-defensin 2 by IL-1β demonstrated that the most proximal NF-κB site on the promoter region of β-defensin 2 was not critical for the process. Data obtained from the normal or patients with the varying ocular diseases showed that our in vitro results were relevant in the clinical settings. Our results clearly demonstrated that β-defensin 1 and 2 are important antimicrobial peptides in the corneal tissues, and that the mechanistic induction process of β-defensin 2 by IL-1β is not solely dependent on proximal NF-κB site activation, thus suggesting that the long distal portion of the promoter is needed for the full responsiveness toward IL-1β.",
keywords = "βdefensins, Antimicrobial cationic peptides, Cornea, Corneal epithelium, Gene expression regulation, Interleukin-1β",
author = "Shin, {Jun Seop} and Kim, {Chan Wha} and Kwon, {Young Sam} and Kim, {Jae Chan}",
year = "2004",
month = "6",
day = "30",
language = "English",
volume = "36",
pages = "204--210",
journal = "Experimental and Molecular Medicine",
issn = "1226-3613",
publisher = "Korean Society of Med. Biochemistry and Mol. Biology",
number = "3",

}

TY - JOUR

T1 - Human β-defensin 2 is induced by interleukin-1β in the corneal epithelial cells

AU - Shin, Jun Seop

AU - Kim, Chan Wha

AU - Kwon, Young Sam

AU - Kim, Jae Chan

PY - 2004/6/30

Y1 - 2004/6/30

N2 - Mammalian epithelia produce the various antimicrobial peptides against the bacterial or viral infection, thereby acting as the active immune modulators in the innate immunity. In this study, we examined the effects of the various proinflammatory cytokines or LPS on cell viability and antimicrobial β-defensin gene expressions in human corneal epithelial cells. Results showed that the cytokines or LPS did not exert severe cytotoxic effects on the cells, and that β-defensin 1 was constitutively expressed, while β-defensin 2 was specifically induced by IL-1β, supporting the idea that these cytokines or LPS involve the defense mechanism in the cornea. Furthermore, the reporter and gel shift assay to define the induction mechanism of β-defensin 2 by IL-1β demonstrated that the most proximal NF-κB site on the promoter region of β-defensin 2 was not critical for the process. Data obtained from the normal or patients with the varying ocular diseases showed that our in vitro results were relevant in the clinical settings. Our results clearly demonstrated that β-defensin 1 and 2 are important antimicrobial peptides in the corneal tissues, and that the mechanistic induction process of β-defensin 2 by IL-1β is not solely dependent on proximal NF-κB site activation, thus suggesting that the long distal portion of the promoter is needed for the full responsiveness toward IL-1β.

AB - Mammalian epithelia produce the various antimicrobial peptides against the bacterial or viral infection, thereby acting as the active immune modulators in the innate immunity. In this study, we examined the effects of the various proinflammatory cytokines or LPS on cell viability and antimicrobial β-defensin gene expressions in human corneal epithelial cells. Results showed that the cytokines or LPS did not exert severe cytotoxic effects on the cells, and that β-defensin 1 was constitutively expressed, while β-defensin 2 was specifically induced by IL-1β, supporting the idea that these cytokines or LPS involve the defense mechanism in the cornea. Furthermore, the reporter and gel shift assay to define the induction mechanism of β-defensin 2 by IL-1β demonstrated that the most proximal NF-κB site on the promoter region of β-defensin 2 was not critical for the process. Data obtained from the normal or patients with the varying ocular diseases showed that our in vitro results were relevant in the clinical settings. Our results clearly demonstrated that β-defensin 1 and 2 are important antimicrobial peptides in the corneal tissues, and that the mechanistic induction process of β-defensin 2 by IL-1β is not solely dependent on proximal NF-κB site activation, thus suggesting that the long distal portion of the promoter is needed for the full responsiveness toward IL-1β.

KW - βdefensins

KW - Antimicrobial cationic peptides

KW - Cornea

KW - Corneal epithelium

KW - Gene expression regulation

KW - Interleukin-1β

UR - http://www.scopus.com/inward/record.url?scp=3242755069&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=3242755069&partnerID=8YFLogxK

M3 - Article

VL - 36

SP - 204

EP - 210

JO - Experimental and Molecular Medicine

JF - Experimental and Molecular Medicine

SN - 1226-3613

IS - 3

ER -