title: Airway inflammation is present during clinical remission of atopic asthma.
abstract: Symptoms of atopic asthma often disappear at puberty. However, asthmatic subjects in clinical remission will frequently have a relapse later in life. The aim of this study was to investigate whether subjects in clinical remission of atopic asthma have persistent airway inflammation and/or airway remodeling. Bronchial biopsies were obtained from subjects in clinical remission, asthmatic subjects, and healthy control subjects. The presence and/or activation state of eosinophils, mast cells, macrophages, T lymphocytes, interleukin (IL)-5, eotaxin, and inducible nitric oxide synthase (iNOS) were analyzed. Results were compared with less invasive indicators of airway inflammation. Also aspects of airway remodeling were determined. Eosinophils, T cells, mast cells, and IL-5 were significantly elevated in the airway mucosa of subjects in remission compared with control subjects. Also, blood eosinophil cell counts were significantly higher in subjects in clinical remission. Blood eosinophil cell counts, exhaled nitric oxide (eNO) levels, and bronchial response to adenosine-5'-monophosphate correlated significantly with the quantity of tissue eosinophils. Significant airway remodeling was found in subjects in clinical remission. Our study has shown ongoing airway inflammation and airway remodeling in adolescents in clinical remission of atopic asthma. Subclinical airway inflammation may well determine the risk of an asthma relapse later in life.
authors.affiliation: Department of Pulmonary Medicine, Erasmus University Medical Center Rotterdam, The Netherlands. L.vandentoorn@planet.nl
authors.forename: L M
authors.initials: LM
authors.lastname: van den Toorn
authors.forename: S E
authors.initials: SE
authors.lastname: Overbeek
authors.forename: J C
authors.initials: JC
authors.lastname: de Jongste
authors.forename: K
authors.initials: K
authors.lastname: Leman
authors.forename: H C
authors.initials: HC
authors.lastname: Hoogsteden
authors.forename: J B
authors.initials: JB
authors.lastname: Prins
mesh_terms: D000249:Adenosine Monophosphate / Q000494:pharmacology; D000293:Adolescent; D000328:Adult; D000367:Age Factors; D001249:Asthma / Q000097:blood / Q000276:immunology* / Q000473:pathology*; D001706:Biopsy; D001944:Breath Tests; D016022:Case-Control Studies; D004804:Eosinophils / Q000276:immunology; D005260:Female; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000097:blood / Q000276:immunology* / Q000473:pathology*; D007150:Immunohistochemistry; D007249:Inflammation; D015848:Interleukin-5 / Q000032:analysis / Q000276:immunology; D007958:Leukocyte Count; D008264:Macrophages / Q000276:immunology; D008297:Male; D008407:Mast Cells / Q000276:immunology; D009569:Nitric Oxide / Q000032:analysis; D012008:Recurrence; D012075:Remission, Spontaneous; D020545:Respiratory Mucosa / Q000737:chemistry / Q000276:immunology* / Q000473:pathology*; D012307:Risk Factors; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D015848:Interleukin-5; D009569:Nitric Oxide; D000249:Adenosine Monophosphate