Document Detail

Modulation of mucus production by interleukin-13 receptor alpha2 in the human airway epithelium.
MedLine Citation:
PMID:  18028464     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: IL-13 induces goblet cell hyperplasia and mucus overproduction in airway epithelial cells. IL-13 receptor alpha2 (IL-13Ralpha(2)) has been suggested to act as a 'decoy receptor' in the airway epithelium by inhibiting the IL-13 signal. However, the regulatory mechanisms for mucus production by IL-13Ralpha(2) remain unclear. OBJECTIVE: The aim of this study was to examine the role of IL-13Ralpha(2) in goblet cell hyperplasia and mucus overproduction by IL-13. METHODS: Bronchi were obtained from patients who underwent a lung resection due to lung cancer or benign lung tumours. Normal human bronchial epithelial cells (NHBECs) were isolated and cultured using an air-liquid interface (ALI) method. RESULTS: The number of periodic acid-Schiff's (PAS)-positive cells, goblet cells and MUC5AC-positive cells increased after adding IL-13 into NHBECs. The concentrations of MUC5AC protein in the supernatant and the mRNA expression of MUC5AC significantly increased after adding IL-13, and returned to control levels at 21 days. The mRNA expression of IL-13Ralpha(2) significantly increased at 7 days and then continuously increased up to 21 days. The protein of a soluble form of IL-13Ralpha(2) in the supernatants significantly increased at 14 and 21 days. Anti-IL-13Ralpha(1) antibody and recombinant IL-13Ralpha(2) reduced the number of PAS-positive cells, goblet cells and MUC5AC-positive cells, and MUC5AC mRNA, while the anti-IL-13Ralpha(2) antibody increased the number of these cells and MUC5AC mRNA. The concentration of MUC5AC protein in the supernatant induced by IL-13 was reduced by anti- IL-13Ralpha(1) antibody and recombinant IL-13Ralpha(2). IL-13-induced signal transducer and activator of transcription (STAT) activation was inhibited by anti-IL-13Ralpha(1) antibody and recombinant IL-13Ralpha(2). In contrast, the IL-4-induced mucus production, mucus secretion and STAT activation were not inhibited by recombinant IL-13Ralpha(2). CONCLUSION: The soluble form of IL-13Ralpha(2) may therefore modulate mucus overproduction by IL-13 through the pathway including IL-13Ralpha(1) in NHBECs.
T Tanabe; K Fujimoto; M Yasuo; K Tsushima; K Yoshida; H Ise; M Yamaya
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-11-19
Journal Detail:
Title:  Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology     Volume:  38     ISSN:  1365-2222     ISO Abbreviation:  Clin. Exp. Allergy     Publication Date:  2008 Jan 
Date Detail:
Created Date:  2007-12-17     Completed Date:  2008-02-01     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  8906443     Medline TA:  Clin Exp Allergy     Country:  England    
Other Details:
Languages:  eng     Pagination:  122-34     Citation Subset:  IM    
Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan.
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MeSH Terms
Aged, 80 and over
Antibodies / immunology
Cells, Cultured
Epithelium / drug effects,  metabolism,  secretion
Gene Expression Regulation / drug effects
Hyperplasia / chemically induced
Interleukin-13 / pharmacology
Interleukin-13 Receptor alpha2 Subunit / genetics,  immunology,  metabolism*
Lung / drug effects,  metabolism*,  secretion
Middle Aged
Mucin 5AC
Mucins / metabolism,  secretion
Mucus / drug effects,  immunology,  metabolism*,  secretion
RNA, Messenger / genetics
Signal Transduction
Time Factors
Transcription, Genetic / genetics
Reg. No./Substance:
0/Antibodies; 0/Interleukin-13; 0/Interleukin-13 Receptor alpha2 Subunit; 0/MUC5AC protein, human; 0/Mucin 5AC; 0/Mucins; 0/RNA, Messenger
Erratum In:
Clin Exp Allergy. 2008 Feb;38(2):382

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