title: Th1 and th2 cytokine expression in nasopharyngeal secretions during acute bronchiolitis in children younger than two years old.
abstract: OBJECTIVE
  We characterised the T helper cytokine profiles on the surface of nasal mucosa of children with acute bronchiolitis caused by Respiratory Syncytial Virus, Parainfluenza Virus, Influenza Virus, Adenovirus, or without any viral identification, in order to examine whether these viral types modified cytokine responses. As an additional objective we sought to determine if T helper polarisation was associated with other demographic and environmental factors.
  
  
  METHODS
  A prospective study of children with acute bronchiolitis was performed. Patients were recruited from the emergency department of a central hospital in Lisbon, Portugal. Demographical, epidemiological and clinical data were gathered from a questionnaire. Nasal swabs were collected for viral studies (immunofluorescence) and T cell cytokine responses (detection of expression of interleukins 4, 13, 12 and interferon-γ by real-time polymerase chain reaction assays).
  
  
  RESULTS
  Respiratory Syncytial Virus elicited lower levels of interleukin 4, when compared with samples without virus identification. A similar tendency to Th1 polarisation was found in older children, in those who attended day-care centres, and in breastfed individuals. Exposure to tobacco smoke was associated with a Th2 bias in this population.
  
  
  CONCLUSIONS
  These findings show that Respiratory Syncytial Virus infection contributes to Th1 polarisation in immune response of respiratory mucosa, an effect that is similar to other environmental factors. Further studies are needed to assess immune response to other infectious causes of acute bronchiolitis.
authors.affiliation: Pediatrics, Hospital S Francisco Xavier, Lisboa, Portugal. pedro.flores@sapo.pt
authors.forename: P
authors.initials: P
authors.lastname: Flores
authors.forename: J
authors.initials: J
authors.lastname: Guimarães
authors.forename: J M
authors.initials: JM
authors.lastname: Videira Amaral
mesh_terms: D000208:Acute Disease; D001990:Bronchiolitis, Viral / Q000453:epidemiology / Q000276:immunology* / Q000821:virology; D016207:Cytokines / Q000235:genetics* / Q000276:immunology; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D015870:Gene Expression / Q000276:immunology; D006801:Humans; D007223:Infant; D007371:Interferon-gamma / Q000235:genetics / Q000276:immunology; D018664:Interleukin-12 / Q000235:genetics / Q000276:immunology; D018793:Interleukin-13 / Q000235:genetics / Q000276:immunology; D015847:Interleukin-4 / Q000235:genetics / Q000276:immunology; D008297:Male; D009297:Nasal Mucosa / Q000276:immunology* / Q000821:virology; D011174:Portugal / Q000453:epidemiology; D011446:Prospective Studies; D018357:Respiratory Syncytial Virus Infections / Q000276:immunology; D018113:Respiratory Syncytial Virus, Human / Q000276:immunology / Q000302:isolation & purification; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012307:Risk Factors; D012720:Severity of Illness Index; D011795:Surveys and Questionnaires; D018417:Th1 Cells / Q000276:immunology* / Q000821:virology; D018418:Th2 Cells / Q000276:immunology* / Q000821:virology
chemical_list: D016207:Cytokines; D018793:Interleukin-13; D018664:Interleukin-12; D015847:Interleukin-4; D007371:Interferon-gamma