title: T cell and eosinophil activation in mild and moderate atopic and nonatopic children's asthma in remission.
abstract: BACKGROUND
  Inflammation in the pathogenesis of asthma is associated with products of activated T cells and eosinophils. The aim of this study was to determine whether ongoing inflammation persists in children with different phenotypes of asthma despite the disease in remission.
  
  
  METHODS
  Serum samples were collected from 68 children with atopic or nonatopic asthma in remission and from 15 healthy children. Soluble interleukin-2 receptor (sIL-2R), IL-2 and IL-4 were examined by using an enzyme-linked immunosorbent assay. Total and specific immunoglobulin E, and eosinophil cationic protein (ECP) were analysed by fluoroimmunoassay (Pharmacia CAP System).
  
  
  RESULTS
  In patients with moderate persistent atopic asthma, sIL-2R was increased significantly when compared with mild persistent atopic asthma (P < 0.05). No changes of sIL-2R were seen in nonatopic asthmatics compared with atopics and controls. The level of IL-2 was elevated in moderate persistent atopic and nonatopic asthmatic children compared with controls (P < 0.05 and P < 0.05 respectively) and compared with mild persistent atopic asthmatics and mild persistent nonatopic asthmatics (P < 0.05 in both cases). The levels of IL-4 in most patients and controls remained below the sensitivity of the assay. Eosinophil cationic protein levels in moderate persistent atopic and nonatopic asthmatics were significantly higher than in mild persistent asthma severity cases (P < 0.001 and P < 0.01 respectively) and in healthy children (P < 0.01 in both cases).
  
  
  CONCLUSIONS
  Changes in the concentration of sIL-2R, IL-2 and ECP reflect increased T cell and eosinophil activity in relation to the level of severity of asthma in atopic and nonatopic children, thereby proving the presence of persistent inflammation despite the absence of disease symptoms.
authors.affiliation: Institute of Immunology, Vilnius University, Vilnius, Lithuania.
authors.forename: I
authors.initials: I
authors.lastname: Pumputiene
authors.forename: R
authors.initials: R
authors.lastname: Emuzyte
authors.forename: R
authors.initials: R
authors.lastname: Dubakiene
authors.forename: R
authors.initials: R
authors.lastname: Firantiene
authors.forename: V
authors.initials: V
authors.lastname: Tamosiunas
mesh_terms: D001249:Asthma / Q000097:blood / Q000276:immunology*; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D002648:Child; D016207:Cytokines / Q000032:analysis* / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay; D004804:Eosinophils / Q000166:cytology / Q000276:immunology*; D005260:Female; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000175:diagnosis / Q000276:immunology*; D007376:Interleukin-2 / Q000032:analysis / Q000276:immunology; D015847:Interleukin-4 / Q000032:analysis / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D011336:Probability; D017472:Receptors, Interleukin-1 / Q000032:analysis / Q000276:immunology; D012016:Reference Values; D012307:Risk Factors; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology*
chemical_list: D015415:Biomarkers; D016207:Cytokines; D007376:Interleukin-2; D017472:Receptors, Interleukin-1; D015847:Interleukin-4