IL-9 and its receptor in allergic and nonallergic lung disease: Increased expression in asthma

Ayako Shimbara, Pota Christodoulopoulos, Abdelilah Soussi-Gounni, Ronald Olivenstein, Yutaka Nakamura, Roy C Levitt, Nicholas C. Nicolaides, Kenneth J. Holroyd, Anne Tsicopoulos, Jean Jacques Lafitte, Benoit Wallaert, Qutayba A. Hamid

Research output: Contribution to journalArticle

209 Citations (Scopus)

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 languageEnglish
Pages (from-to)108-115
Number of pages8
JournalJournal of Allergy and Clinical Immunology
Volume105
Issue number1 I
StatePublished - Feb 1 2000
Externally publishedYes

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Interleukin-9 Receptors
Interleukin-9
Lung Diseases
Asthma
Messenger RNA
In Situ Hybridization
Eosinophil Major Basic Protein
Immunohistochemistry
Leukocyte Elastase
Methacholine Chloride
Chronic Bronchitis
Sarcoidosis
Immunoglobulin E
Healthy Volunteers
Chronic Disease
Lymphocytes
Cytokines
Phenotype
Biopsy

Keywords

  • Asthma
  • Atopy
  • IL-9
  • IL-9 receptor

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Shimbara, A., Christodoulopoulos, P., Soussi-Gounni, A., Olivenstein, R., Nakamura, Y., Levitt, R. C., ... Hamid, Q. A. (2000). IL-9 and its receptor in allergic and nonallergic lung disease: Increased expression in asthma. Journal of Allergy and Clinical Immunology, 105(1 I), 108-115.

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 journalArticle

Shimbara, A, Christodoulopoulos, P, Soussi-Gounni, A, Olivenstein, R, Nakamura, Y, Levitt, RC, Nicolaides, NC, Holroyd, KJ, Tsicopoulos, A, Lafitte, JJ, Wallaert, B & Hamid, QA 2000, 'IL-9 and its receptor in allergic and nonallergic lung disease: Increased expression in asthma', Journal of Allergy and Clinical Immunology, vol. 105, no. 1 I, pp. 108-115.
Shimbara A, Christodoulopoulos P, Soussi-Gounni A, Olivenstein R, Nakamura Y, Levitt RC et al. IL-9 and its receptor in allergic and nonallergic lung disease: Increased expression in asthma. Journal of Allergy and Clinical Immunology. 2000 Feb 1;105(1 I):108-115.
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. / IL-9 and its receptor in allergic and nonallergic lung disease : Increased expression in asthma. In: Journal of Allergy and Clinical Immunology. 2000 ; Vol. 105, No. 1 I. pp. 108-115.
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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.",
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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.

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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.

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