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 language | English (US) |
|---|---|
| Pages (from-to) | 93-98 |
| Number of pages | 6 |
| Journal | Journal of Organ Dysfunction |
| Volume | 4 |
| Issue number | 2 |
| DOIs | |
| State | Published - 2008 |
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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 journal › Article
}
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 -