|
|
||||||||
Guest Access | Sign In via User Name/Password |
|||||||||
* From the Fraunhofer Institute of Toxicology and Aerosol Research (Drs. Erpenbeck, Braun, and Krug), Hannover; and Department of Respiratory Medicine (Mr. Discher, Mr. Krentel, and Ms. Hagenberg), Hannover Medical School, Hannover, Germany.
Correspondence to: Veit J. Erpenbeck, Nikolai-Fuchs-Strasse 1a, D-30625 Hannover, Germany; e-mail: erpenbeck{at}ita.fraunhofer.de
Cytokine production by T cells and eosinophils plays a major role in allergic asthma. Both cell types produce interleukin (IL)-9, which belongs to the group of T-helper type 2 cytokines comprising IL-4, IL-5, and IL-13. It shares genetic as well as functional similarities with these cytokines and may therefore contribute to the pathogenesis of allergic disorders such as bronchial asthma. To investigate the relevance of IL-9 for the formation of the allergic response, we measured the expression of IL-9 messenger RNA of cells obtained from BAL before and 24 h after segmental allergen and saline solution challenge of 10 subjects with mild asthma and 5 healthy control subjects. Following processing of cells, messenger RNA expression of IL-9 and porphobilinogen deaminase as a housekeeping gene was measured using real-time polymerase chain reaction with the Lightcycler (Roche Diagnostics; Mannheim, Germany). Relative quantification of IL-9 messenger RNA was performed vs the housekeeping gene porphobilinogen deaminase.
There was an increased expression of IL-9 messenger RNA after segmental allergen provocation in asthmatics (p < 0.01). This difference did not occur after saline solution provocation or after allergen provocation of healthy control subjects. The increase of IL-9 messenger RNA expression after allergen provocation in asthmatics points to the importance of this cytokine for the pathophysiologic changes in allergic diseases.
| Footnotes |
|---|
Supported by Deutsche Forschungsgemeinschaft grant Kr1405/2-2.
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |