title: Natural killer T cells are dispensable in the development of allergen-induced airway hyperresponsiveness, inflammation and remodelling in a mouse model of chronic asthma.
abstract: Natural killer T (NK T) cells have been shown to play an essential role in the development of allergen-induced airway hyperresponsiveness (AHR) and/or airway inflammation in mouse models of acute asthma. Recently, NK T cells have been reported to be required for the development of AHR in a virus induced chronic asthma model. We investigated whether NK T cells were required for the development of allergen-induced AHR, airway inflammation and airway remodelling in a mouse model of chronic asthma. CD1d-/- mice that lack NK T cells were used for the experiments. In the chronic model, AHR, eosinophilic inflammation, remodelling characteristics including mucus metaplasia, subepithelial fibrosis and increased mass of the airway smooth muscle, T helper type 2 (Th2) immune response and immunoglobulin (Ig)E production were equally increased in both CD1d-/- mice and wild-type mice. However, in the acute model, AHR, eosinophilic inflammation, Th2 immune response and IgE production were significantly decreased in the CD1d-/- mice compared to wild-type. CD1d-dependent NK T cells may not be required for the development of allergen-induced AHR, eosinophilic airway inflammation and airway remodelling in chronic asthma model, although they play a role in the development of AHR and eosinophilic inflammation in acute asthma model.
authors.affiliation: Department of Allergy, Asthma and Clinical Immunology and Research Institute of Medical Sciences, Chonnam National University Medical School, Gwangju, South Korea. yikoh@chonnam.ac.kr
authors.forename: Y-I
authors.initials: YI
authors.lastname: Koh
authors.forename: J-U
authors.initials: JU
authors.lastname: Shim
authors.forename: J-H
authors.initials: JH
authors.lastname: Lee
authors.forename: I-J
authors.initials: IJ
authors.lastname: Chung
authors.forename: J-J
authors.initials: JJ
authors.lastname: Min
authors.forename: J H
authors.initials: JH
authors.lastname: Rhee
authors.forename: H C
authors.initials: HC
authors.lastname: Lee
authors.forename: D H
authors.initials: DH
authors.lastname: Chung
authors.forename: J-O
authors.initials: JO
authors.lastname: Wi
mesh_terms: D000208:Acute Disease; D056151:Airway Remodeling / Q000276:immunology*; D000403:Airway Resistance; D000485:Allergens / Q000633:toxicity*; D000818:Animals; D055610:Antigens, CD1d / Q000235:genetics; D001249:Asthma; D016535:Bronchial Hyperreactivity / Q000209:etiology / Q000276:immunology*; D001991:Bronchitis / Q000209:etiology / Q000276:immunology*; D002908:Chronic Disease; D004195:Disease Models, Animal; D005260:Female; D005355:Fibrosis; D007073:Immunoglobulin E / Q000096:biosynthesis / Q000235:genetics; D008297:Male; D008679:Metaplasia; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D009130:Muscle, Smooth / Q000473:pathology; D055611:Natural Killer T-Cells / Q000276:immunology*; D010047:Ovalbumin / Q000276:immunology / Q000633:toxicity; D011657:Pulmonary Eosinophilia / Q000209:etiology; D018418:Th2 Cells / Q000276:immunology
chemical_list: D000485:Allergens; D055610:Antigens, CD1d; D007073:Immunoglobulin E; D010047:Ovalbumin
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