Abstract
Background: Bronchial asthma is a chronic inflammatory disease associated with genetic components. Recently IL-9 has been reported as a candidate gene for asthma and to be associated with bronchial hyperresponsiveness and elevated levels of total serum IgE. Objective: To investigate the contribution of IL-9 to the pathogenesis of asthma, we examined the expression of IL-9 and its receptor (IL-9R) in bronchial tissue from subjects with atopic asthma (n = 10), chronic bronchitis (n = 11), and sarcoidosis (n = 9) and from atopic (n = 7) and nonatopic (n = 10) healthy control subjects. Methods: Bronchial biopsy specimens were examined for the presence of IL-9 and IL-9R protein and messenger RNA (mRNA) by immunocytochemistry and in situ hybridization, respectively. To phenotype the cells expressing IL-9 in asthmatic tissue, combined in situ hybridization and immunocytochemistry was also performed. Results: There was a highly significant difference (P < .001) in the expression of IL-9 mRNA in asthmatic airways (20.6 ± 4.0 cells/mm of basement membrane) compared with chronic bronchitis (5.6 ± 4.4), sarcoidosis (2.5 ± 1.8), atopic control subjects (7.7 ± 2.2), and healthy control subjects (2.7 ± 2.3). The number of IL-9 immunoreactive cells was also greater in asthmatic patients compared with the other groups (P < .05). Although the level of IL-9R mRNA expression did not differ in any of the groups (P > .05), IL-9R immunoreactivity was significantly higher in asthmatic compared with control subjects. Furthermore, IL-9 mRNA expression levels were also significantly correlated with FEV1 (P < .05) and the airway responsiveness to methacholine producing a 20% fall in FEV1 (P < .01). The cells expressing IL-9 mRNA in asthmatic tissue were CD3+ lymphocytes (68%), major basic protein+ eosinophils (16%), and elastase+ neutrophils (8%). Conclusion: The results of this study demonstrate the potential of IL-9 to be a marker for atopic asthma and furthermore suggest an important role for this cytokine in the pathophysiologic mechanisms of this disease.
| Original language | English |
|---|---|
| Pages (from-to) | 108-115 |
| Number of pages | 8 |
| Journal | Journal of Allergy and Clinical Immunology |
| Volume | 105 |
| Issue number | 1 I |
| State | Published - Feb 1 2000 |
| Externally published | Yes |
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Keywords
- Asthma
- Atopy
- IL-9
- IL-9 receptor
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
Cite this
IL-9 and its receptor in allergic and nonallergic lung disease : Increased expression in asthma. / Shimbara, Ayako; Christodoulopoulos, Pota; Soussi-Gounni, Abdelilah; Olivenstein, Ronald; Nakamura, Yutaka; Levitt, Roy C; Nicolaides, Nicholas C.; Holroyd, Kenneth J.; Tsicopoulos, Anne; Lafitte, Jean Jacques; Wallaert, Benoit; Hamid, Qutayba A.
In: Journal of Allergy and Clinical Immunology, Vol. 105, No. 1 I, 01.02.2000, p. 108-115.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - IL-9 and its receptor in allergic and nonallergic lung disease
T2 - Increased expression in asthma
AU - Shimbara, Ayako
AU - Christodoulopoulos, Pota
AU - Soussi-Gounni, Abdelilah
AU - Olivenstein, Ronald
AU - Nakamura, Yutaka
AU - Levitt, Roy C
AU - Nicolaides, Nicholas C.
AU - Holroyd, Kenneth J.
AU - Tsicopoulos, Anne
AU - Lafitte, Jean Jacques
AU - Wallaert, Benoit
AU - Hamid, Qutayba A.
PY - 2000/2/1
Y1 - 2000/2/1
N2 - Background: Bronchial asthma is a chronic inflammatory disease associated with genetic components. Recently IL-9 has been reported as a candidate gene for asthma and to be associated with bronchial hyperresponsiveness and elevated levels of total serum IgE. Objective: To investigate the contribution of IL-9 to the pathogenesis of asthma, we examined the expression of IL-9 and its receptor (IL-9R) in bronchial tissue from subjects with atopic asthma (n = 10), chronic bronchitis (n = 11), and sarcoidosis (n = 9) and from atopic (n = 7) and nonatopic (n = 10) healthy control subjects. Methods: Bronchial biopsy specimens were examined for the presence of IL-9 and IL-9R protein and messenger RNA (mRNA) by immunocytochemistry and in situ hybridization, respectively. To phenotype the cells expressing IL-9 in asthmatic tissue, combined in situ hybridization and immunocytochemistry was also performed. Results: There was a highly significant difference (P < .001) in the expression of IL-9 mRNA in asthmatic airways (20.6 ± 4.0 cells/mm of basement membrane) compared with chronic bronchitis (5.6 ± 4.4), sarcoidosis (2.5 ± 1.8), atopic control subjects (7.7 ± 2.2), and healthy control subjects (2.7 ± 2.3). The number of IL-9 immunoreactive cells was also greater in asthmatic patients compared with the other groups (P < .05). Although the level of IL-9R mRNA expression did not differ in any of the groups (P > .05), IL-9R immunoreactivity was significantly higher in asthmatic compared with control subjects. Furthermore, IL-9 mRNA expression levels were also significantly correlated with FEV1 (P < .05) and the airway responsiveness to methacholine producing a 20% fall in FEV1 (P < .01). The cells expressing IL-9 mRNA in asthmatic tissue were CD3+ lymphocytes (68%), major basic protein+ eosinophils (16%), and elastase+ neutrophils (8%). Conclusion: The results of this study demonstrate the potential of IL-9 to be a marker for atopic asthma and furthermore suggest an important role for this cytokine in the pathophysiologic mechanisms of this disease.
AB - Background: Bronchial asthma is a chronic inflammatory disease associated with genetic components. Recently IL-9 has been reported as a candidate gene for asthma and to be associated with bronchial hyperresponsiveness and elevated levels of total serum IgE. Objective: To investigate the contribution of IL-9 to the pathogenesis of asthma, we examined the expression of IL-9 and its receptor (IL-9R) in bronchial tissue from subjects with atopic asthma (n = 10), chronic bronchitis (n = 11), and sarcoidosis (n = 9) and from atopic (n = 7) and nonatopic (n = 10) healthy control subjects. Methods: Bronchial biopsy specimens were examined for the presence of IL-9 and IL-9R protein and messenger RNA (mRNA) by immunocytochemistry and in situ hybridization, respectively. To phenotype the cells expressing IL-9 in asthmatic tissue, combined in situ hybridization and immunocytochemistry was also performed. Results: There was a highly significant difference (P < .001) in the expression of IL-9 mRNA in asthmatic airways (20.6 ± 4.0 cells/mm of basement membrane) compared with chronic bronchitis (5.6 ± 4.4), sarcoidosis (2.5 ± 1.8), atopic control subjects (7.7 ± 2.2), and healthy control subjects (2.7 ± 2.3). The number of IL-9 immunoreactive cells was also greater in asthmatic patients compared with the other groups (P < .05). Although the level of IL-9R mRNA expression did not differ in any of the groups (P > .05), IL-9R immunoreactivity was significantly higher in asthmatic compared with control subjects. Furthermore, IL-9 mRNA expression levels were also significantly correlated with FEV1 (P < .05) and the airway responsiveness to methacholine producing a 20% fall in FEV1 (P < .01). The cells expressing IL-9 mRNA in asthmatic tissue were CD3+ lymphocytes (68%), major basic protein+ eosinophils (16%), and elastase+ neutrophils (8%). Conclusion: The results of this study demonstrate the potential of IL-9 to be a marker for atopic asthma and furthermore suggest an important role for this cytokine in the pathophysiologic mechanisms of this disease.
KW - Asthma
KW - Atopy
KW - IL-9
KW - IL-9 receptor
UR - http://www.scopus.com/inward/record.url?scp=4444262198&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=4444262198&partnerID=8YFLogxK
M3 - Article
C2 - 10629460
AN - SCOPUS:4444262198
VL - 105
SP - 108
EP - 115
JO - Journal of Allergy and Clinical Immunology
JF - Journal of Allergy and Clinical Immunology
SN - 0091-6749
IS - 1 I
ER -