Regulation of mucosal immunity by airway epithelium: The interleukin-17A paradigm

Fei Huang, Cheng Yuan Kao, Philip Thai, Shinichiro Wachi, Christy Kim, Yong Lee, Li Yin Hung, Richart W Harper, Mary Mann-Jong Chang, Reen Wu

Research output: Contribution to journalArticle

Abstract

Increasing evidence suggests that the airway epithelium plays an essential role in the modulation of airway innate and adaptive immune responses in addition to serving as a physical barrier against microbial infection and exterior insults. The nature of this modulation and the potential mediators involved are currently unresolved. Interleukin (IL)-17A has recently emerged as a potential candidate for directly modulating innate and adaptive immune responses. Our laboratory has recently shown that IL-17A is one of the most potent cytokines among a panel of 21 (IL-1α, -1β, -2-13, -15, -16, and -18, interferon-γ, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor-α) for stimulating the expression of human β-defensin (HBD)-2 and CC chemokine ligand 20 (CCL20)/macrophage inflammatory protein-3 by primary human airway epithelial cells. Using Affymetrix gene chips and quantitative polymerase chain reaction, we identified the following IL-17A-induced genes in well-differentiated normal human bronchial epithelium: IL-19, growth-related oncogene-α, -β, and -γ, CXC-5, and glutamate carboxypeptidase-2, in addition to the known inducible cytokines CCL20, IL-8, and HBD-2. As the presence of IL-17A at elevated levels has been demonstrated in a variety of airway diseases, including those related to microbial infection, chronic obstructive pulmonary disease, and Th2-dominated diseases, the induction of these diverse cytokines may further support the critical role of IL-17A in the pathogenesis of airway diseases and airway inflammation.

Original languageEnglish (US)
Pages (from-to)93-98
Number of pages6
JournalJournal of Organ Dysfunction
Volume4
Issue number2
DOIs
StatePublished - 2008

Fingerprint

Mucosal Immunity
Interleukin-17
Epithelium
CC Chemokines
Adaptive Immunity
Cytokines
Innate Immunity
Ligands
Defensins
Macrophage Inflammatory Proteins
Architectural Accessibility
Interleukins
Granulocyte-Macrophage Colony-Stimulating Factor
Infection
Oligonucleotide Array Sequence Analysis
Interleukin-8
Interleukin-1
Oncogenes
Chronic Obstructive Pulmonary Disease
Interferons

Keywords

  • Airway epithelium
  • Cytokines
  • Interleukin-17A
  • Mucosal immunity

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine
  • Critical Care
  • Physiology
  • Molecular Biology

Cite this

Regulation of mucosal immunity by airway epithelium : The interleukin-17A paradigm. / Huang, Fei; Kao, Cheng Yuan; Thai, Philip; Wachi, Shinichiro; Kim, Christy; Lee, Yong; Hung, Li Yin; Harper, Richart W; Mann-Jong Chang, Mary; Wu, Reen.

In: Journal of Organ Dysfunction, Vol. 4, No. 2, 2008, p. 93-98.

Research output: Contribution to journalArticle

Huang, F, Kao, CY, Thai, P, Wachi, S, Kim, C, Lee, Y, Hung, LY, Harper, RW, Mann-Jong Chang, M & Wu, R 2008, 'Regulation of mucosal immunity by airway epithelium: The interleukin-17A paradigm', Journal of Organ Dysfunction, vol. 4, no. 2, pp. 93-98. https://doi.org/10.1080/17471060701226175
Huang, Fei ; Kao, Cheng Yuan ; Thai, Philip ; Wachi, Shinichiro ; Kim, Christy ; Lee, Yong ; Hung, Li Yin ; Harper, Richart W ; Mann-Jong Chang, Mary ; Wu, Reen. / Regulation of mucosal immunity by airway epithelium : The interleukin-17A paradigm. In: Journal of Organ Dysfunction. 2008 ; Vol. 4, No. 2. pp. 93-98.
@article{564a3a8be8b74b25aa1eac90d3b887e4,
title = "Regulation of mucosal immunity by airway epithelium: The interleukin-17A paradigm",
abstract = "Increasing evidence suggests that the airway epithelium plays an essential role in the modulation of airway innate and adaptive immune responses in addition to serving as a physical barrier against microbial infection and exterior insults. The nature of this modulation and the potential mediators involved are currently unresolved. Interleukin (IL)-17A has recently emerged as a potential candidate for directly modulating innate and adaptive immune responses. Our laboratory has recently shown that IL-17A is one of the most potent cytokines among a panel of 21 (IL-1α, -1β, -2-13, -15, -16, and -18, interferon-γ, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor-α) for stimulating the expression of human β-defensin (HBD)-2 and CC chemokine ligand 20 (CCL20)/macrophage inflammatory protein-3 by primary human airway epithelial cells. Using Affymetrix gene chips and quantitative polymerase chain reaction, we identified the following IL-17A-induced genes in well-differentiated normal human bronchial epithelium: IL-19, growth-related oncogene-α, -β, and -γ, CXC-5, and glutamate carboxypeptidase-2, in addition to the known inducible cytokines CCL20, IL-8, and HBD-2. As the presence of IL-17A at elevated levels has been demonstrated in a variety of airway diseases, including those related to microbial infection, chronic obstructive pulmonary disease, and Th2-dominated diseases, the induction of these diverse cytokines may further support the critical role of IL-17A in the pathogenesis of airway diseases and airway inflammation.",
keywords = "Airway epithelium, Cytokines, Interleukin-17A, Mucosal immunity",
author = "Fei Huang and Kao, {Cheng Yuan} and Philip Thai and Shinichiro Wachi and Christy Kim and Yong Lee and Hung, {Li Yin} and Harper, {Richart W} and {Mann-Jong Chang}, Mary and Reen Wu",
year = "2008",
doi = "10.1080/17471060701226175",
language = "English (US)",
volume = "4",
pages = "93--98",
journal = "Journal of Organ Dysfunction",
issn = "1747-1060",
publisher = "Informa Healthcare",
number = "2",

}

TY - JOUR

T1 - Regulation of mucosal immunity by airway epithelium

T2 - The interleukin-17A paradigm

AU - Huang, Fei

AU - Kao, Cheng Yuan

AU - Thai, Philip

AU - Wachi, Shinichiro

AU - Kim, Christy

AU - Lee, Yong

AU - Hung, Li Yin

AU - Harper, Richart W

AU - Mann-Jong Chang, Mary

AU - Wu, Reen

PY - 2008

Y1 - 2008

N2 - Increasing evidence suggests that the airway epithelium plays an essential role in the modulation of airway innate and adaptive immune responses in addition to serving as a physical barrier against microbial infection and exterior insults. The nature of this modulation and the potential mediators involved are currently unresolved. Interleukin (IL)-17A has recently emerged as a potential candidate for directly modulating innate and adaptive immune responses. Our laboratory has recently shown that IL-17A is one of the most potent cytokines among a panel of 21 (IL-1α, -1β, -2-13, -15, -16, and -18, interferon-γ, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor-α) for stimulating the expression of human β-defensin (HBD)-2 and CC chemokine ligand 20 (CCL20)/macrophage inflammatory protein-3 by primary human airway epithelial cells. Using Affymetrix gene chips and quantitative polymerase chain reaction, we identified the following IL-17A-induced genes in well-differentiated normal human bronchial epithelium: IL-19, growth-related oncogene-α, -β, and -γ, CXC-5, and glutamate carboxypeptidase-2, in addition to the known inducible cytokines CCL20, IL-8, and HBD-2. As the presence of IL-17A at elevated levels has been demonstrated in a variety of airway diseases, including those related to microbial infection, chronic obstructive pulmonary disease, and Th2-dominated diseases, the induction of these diverse cytokines may further support the critical role of IL-17A in the pathogenesis of airway diseases and airway inflammation.

AB - Increasing evidence suggests that the airway epithelium plays an essential role in the modulation of airway innate and adaptive immune responses in addition to serving as a physical barrier against microbial infection and exterior insults. The nature of this modulation and the potential mediators involved are currently unresolved. Interleukin (IL)-17A has recently emerged as a potential candidate for directly modulating innate and adaptive immune responses. Our laboratory has recently shown that IL-17A is one of the most potent cytokines among a panel of 21 (IL-1α, -1β, -2-13, -15, -16, and -18, interferon-γ, granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor-α) for stimulating the expression of human β-defensin (HBD)-2 and CC chemokine ligand 20 (CCL20)/macrophage inflammatory protein-3 by primary human airway epithelial cells. Using Affymetrix gene chips and quantitative polymerase chain reaction, we identified the following IL-17A-induced genes in well-differentiated normal human bronchial epithelium: IL-19, growth-related oncogene-α, -β, and -γ, CXC-5, and glutamate carboxypeptidase-2, in addition to the known inducible cytokines CCL20, IL-8, and HBD-2. As the presence of IL-17A at elevated levels has been demonstrated in a variety of airway diseases, including those related to microbial infection, chronic obstructive pulmonary disease, and Th2-dominated diseases, the induction of these diverse cytokines may further support the critical role of IL-17A in the pathogenesis of airway diseases and airway inflammation.

KW - Airway epithelium

KW - Cytokines

KW - Interleukin-17A

KW - Mucosal immunity

UR - http://www.scopus.com/inward/record.url?scp=45849108802&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=45849108802&partnerID=8YFLogxK

U2 - 10.1080/17471060701226175

DO - 10.1080/17471060701226175

M3 - Article

AN - SCOPUS:45849108802

VL - 4

SP - 93

EP - 98

JO - Journal of Organ Dysfunction

JF - Journal of Organ Dysfunction

SN - 1747-1060

IS - 2

ER -