title: Airway remodeling and inflammation in symptomatic infants with reversible airflow obstruction.
abstract: BACKGROUND
  We hypothesized that the epithelial reticular basement membrane (RBM) thickening and eosinophilic inflammation characteristic of asthma would be present in symptomatic infants with reversible airflow obstruction.
  
  
  METHODS
  RBM thickness and numbers of inflammatory cells were determined in ultrathin sections of endobronchial biopsies obtained from 53 infants during clinical bronchoscopy for severe wheeze and/or cough. Group A: 16 infants with a median age of 12 months (range 3.4-26 months), with decreased specific airway conductance (sGaw) and bronchodilator reversibility; Group B: 22 infants with a median age of 12.4 months (5.1-25.9 months), with decreased sGaw but without bronchodilator reversibility; and Group C: 15 infants with a median age of 11.5 months (3.4-24.3 months) with normal sGaw. Additional comparisons were made with the following groups. Group D: 17 children, median age 10.3 years (6-16 years), with difficult asthma; Group E: 10 pediatric control subjects without asthma, median age 10 years (6-16 years); and Group F: nine adult normal, healthy control subjects, median age 27 years (21-42 years).
  
  
  RESULTS
  There were no significant differences in RBM thickness or inflammatory cell number between the infant groups. RBM thickness was similar in the infants and Groups E and F. However, the RBM in all infant groups (Group A: median 4.3 microm [range 2.8-9.2 microm]; Group B: median 4.15 microm [range 2.7-5.8 microm]; Group C: median 3.8 microm [range 2.7-5.5 microm]) was significantly less thick than that in the older children with asthma (Group D: median 8.3 microm [range 5.3-12.7 microm]; p < 0.001).
  
  
  CONCLUSIONS
  RBM thickening and the eosinophilic inflammation characteristic of asthma in older children and adults are not present in symptomatic infants with reversible airflow obstruction, even in the presence of atopy.
authors.affiliation: Lung Pathology, Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK.
authors.forename: Sejal
authors.initials: S
authors.lastname: Saglani
authors.forename: Kristiina
authors.initials: K
authors.lastname: Malmström
authors.forename: Anna S
authors.initials: AS
authors.lastname: Pelkonen
authors.forename: L Pekka
authors.initials: LP
authors.lastname: Malmberg
authors.forename: Harry
authors.initials: H
authors.lastname: Lindahl
authors.forename: Merja
authors.initials: M
authors.lastname: Kajosaari
authors.forename: Markku
authors.initials: M
authors.lastname: Turpeinen
authors.forename: Andrew V
authors.initials: AV
authors.lastname: Rogers
authors.forename: Donald N
authors.initials: DN
authors.lastname: Payne
authors.forename: Andrew
authors.initials: A
authors.lastname: Bush
authors.forename: Tari
authors.initials: T
authors.lastname: Haahtela
authors.forename: Mika J
authors.initials: MJ
authors.lastname: Mäkelä
authors.forename: Peter K
authors.initials: PK
authors.lastname: Jeffery
mesh_terms: D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000402:Airway Obstruction / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology; D018927:Anti-Asthmatic Agents / Q000627:therapeutic use; D001249:Asthma / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology*; D001485:Basement Membrane / Q000473:pathology; D001707:Biopsy, Needle; D016535:Bronchial Hyperreactivity / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology; D001999:Bronchoscopy; D016022:Case-Control Studies; D002675:Child, Preschool; D015331:Cohort Studies; D018450:Disease Progression; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007223:Infant; D007249:Inflammation / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D011336:Probability; D011379:Prognosis; D018570:Risk Assessment; D012737:Sex Factors
chemical_list: D018927:Anti-Asthmatic Agents