Involvement of IL-9 in the bronchial phenotype of patients with nasal polyposis.
BACKGROUND
Nasal polyposis (NP) is frequently associated with asthma. In this disease, asymptomatic bronchial hyperresponsiveness (BHR) is thought to precede the development of asthma. IL-9 and its receptor have been reported as candidate genes for asthma and to be associated with BHR.


OBJECTIVE
The objective of this study was to assess the contribution of 11-9 to the pathogenesis of BHR in NP by comparing the expression of IL-9 and its receptor in bronchial biopsy specimens from three groups of patients with NP: NP without BHR, NP with asymptomatic BHR, and NP with BHR and asthma.


METHODS
Bronchial biopsy specimens were examined in terms of cellular infiltration and in terms of expression of IL-9 protein and mRNA as well as of its receptor by using immunohistochemistry and in situ hybridization.


RESULTS
Patients with NP with asthma as compared with the two other groups exhibited an increased bronchial infiltration of basophils, eosinophils, and T cells that correlated with the asthma score. The two groups of patients with NP with BHR showed an increased expression in IL-9 protein and mRNA as well as an increase in the expression of IL-9R mRNA at the epithelial level. These modifications were inversely correlated with the airway responsiveness to methacholine, producing a 20% fall in FEV1. There was a close association between IL-9+ cells, IL-5 mRNA expression, and eosinophil infiltration that correlated with each other.


CONCLUSIONS
These results suggest an important role for IL-9 in the pathogenesis of BHR and a causal relation between IL-9 and the development of bronchial eosinophilia in asthma.
INSERM U416, Institut Pasteur de Lille, France.
Anne
A
Tsicopoulos
Ayako
A
Shimbara
Patricia
P
de Nadai
Oday
O
Aldewachi
Catherine
C
Lamblin
Philippe
P
Lassalle
Andrew F
AF
Walls
Stéphanie
S
Sénéchal
Roy C
RC
Levitt
Jean
J
Darras
Qutayba
Q
Hamid
Benoît
B
Wallaert
D000328:Adult; D001249:Asthma / Q000209:etiology / Q000235:genetics / Q000276:immunology / Q000473:pathology; D001491:Basophils / Q000276:immunology / Q000473:pathology; D001980:Bronchi / Q000276:immunology / Q000473:pathology; D016535:Bronchial Hyperreactivity / Q000209:etiology / Q000235:genetics / Q000276:immunology; D004802:Eosinophilia / Q000209:etiology / Q000235:genetics / Q000276:immunology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D015848:Interleukin-5 / Q000235:genetics; D016906:Interleukin-9 / Q000235:genetics / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009298:Nasal Polyps / Q000150:complications / Q000235:genetics / Q000276:immunology*; D010641:Phenotype; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D018123:Receptors, Interleukin / Q000235:genetics / Q000378:metabolism; D053651:Receptors, Interleukin-9; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology
C508045:IL9R protein, human; D015848:Interleukin-5; D016906:Interleukin-9; D012333:RNA, Messenger; D018123:Receptors, Interleukin; D053651:Receptors, Interleukin-9