title: Airway function correlates with circulating eosinophil, but not mast cell, markers of inflammation in childhood asthma.
abstract: BACKGROUND
  Lung function tests, including forced expiratory volume in one second (FEV1), forced expiratory flow at 25-75% of vital capacity (FEF25-75%) and provocation concentrations of histamine which reduce FEV1 by 20% (PC20), are used as indicators of airway form and function in bronchial asthma. Recently, markers of eosinophil activation in bronchial lavage and serum have been suggested as a measure of eosinophil mediated inflammation in the airways. These include eosinophil cationic protein (ECP), eosinophil protein X (EPX) (also known as eosinophil derived neurotoxin) and eosinophil peroxidase (EPO). Similarly, serum tryptase has been used as a marker of mast cell activation in systemic anaphylaxis.
  
  
  OBJECTIVE
  We measured both sets of indices in a group of children with moderately severe asthma to assess the contribution of eosinophil and mast cell mediated events to airflow limitation and bronchial hyperresponsiveness.
  
  
  METHODS
  Forty-eight children aged 5-10 years had spirometric assessments, histamine challenges and blood sampling on the same occasion. After analysis of sera, the indices were compared.
  
  
  RESULTS
  The eosinophil markers ECP and EPX correlated very well with each other. They showed a moderate negative correlation with PC20 for histamine. EPX was also found to negatively correlate with FEV1 and FEF25-75%. Serum tryptase levels showed no such correlates with airway function.
  
  
  CONCLUSIONS
  These results suggest that serum markers of eosinophil activation correlate with airway function in childhood asthma, and may be of value in assessing the severity of the disease. It further supports the notion that childhood asthma has a similar immunopathology to that occurring in adults, with predominance of eosinophil mediated inflammation.
authors.affiliation: Southampton General Hospital, UK.
authors.forename: R
authors.initials: R
authors.lastname: Rao
authors.forename: J M
authors.initials: JM
authors.lastname: Frederick
authors.forename: I
authors.initials: I
authors.lastname: Enander
authors.forename: R K
authors.initials: RK
authors.lastname: Gregson
authors.forename: J A
authors.initials: JA
authors.lastname: Warner
authors.forename: J O
authors.initials: JO
authors.lastname: Warner
mesh_terms: D001249:Asthma / Q000378:metabolism* / Q000503:physiopathology*; D015415:Biomarkers; D001798:Blood Proteins / Q000378:metabolism; D001980:Bronchi / Q000503:physiopathology*; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D002452:Cell Count; D002648:Child; D002675:Child, Preschool; D053818:Chymases; D047091:Eosinophil Granule Proteins; D047209:Eosinophil Peroxidase; D047208:Eosinophil-Derived Neurotoxin; D004804:Eosinophils / Q000378:metabolism* / Q000473:pathology; D005541:Forced Expiratory Volume; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D008407:Mast Cells / Q000378:metabolism; D008450:Maximal Midexpiratory Flow Rate; D010544:Peroxidases / Q000378:metabolism; D012260:Ribonucleases; D012697:Serine Endopeptidases / Q000097:blood; D053802:Tryptases
chemical_list: D015415:Biomarkers; D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D018836:Inflammation Mediators; D047209:Eosinophil Peroxidase; D010544:Peroxidases; D047208:Eosinophil-Derived Neurotoxin; D012260:Ribonucleases; D012697:Serine Endopeptidases; C083294:chymase 2; D053818:Chymases; D053802:Tryptases