title: Pro-inflammatory and Th2-type cytokine responses in PBMC in infants are associated with parental smoking.
abstract: BACKGROUND
  During infancy, a disturbed cytokine balance leads to an atopic immune response. Many risk factors have been associated with the development of atopy. These include parental smoking, elevated cord blood IgE, early exposure to pets and family history of atopy, but the knowledge of their impact on cytokine balance is limited.
  
  
  OBJECTIVE
  To assess the cytokines induced by mitogen in peripheral blood mononuclear cells (PBMC) of infants at 3 months and 12 months of age and their potential association with fatty acid (FA) intervention, parental atopy, atopic dermatitis and parental smoking.
  
  
  METHODS
  Infants from an intervention study using black currant seed oil (BCSO, n = 34) or placebo (n = 34) were included. PBMC samples were taken at the age of 3 and 12 months. Signs of atopic dermatitis and parental smoking were registered. PBMC were isolated from heparinized blood samples, stimulated with ConcanavalinA mitogen and the cytokine responses were detected at 72 h of stimulation by Luminex technology.
  
  
  RESULTS
  Children of smoking parents had elevated levels of IL-4 (P = 0.0004), IL-5 (P = 0.0002), IFN-γ (P = 0.039) and TNF (P = 0.0003) at 12 months of age. Children who had atopic dermatitis by the age of 3 months showed elevated levels of IL-5 at 3 months (P = 0.0027) and 12 months of age (P = 0.022). The production of TNF at the age of 3 months was higher (P = 0.010) and the production of IL-12 at the age of 12 months was lower (P = 0.025) in infants whose parents were atopic. BCSO intervention did not have any effect on any cytokine production or mRNA expression.
  
  
  CONCLUSIONS
  Children of smoking parents had highly significantly elevated levels of Th2-type cytokines IL-4, IL-5 and pro-inflammatory cytokine TNF. The detrimental effects of parental smoking on the child's immune function should lead us to pay more attention to supporting parents to stop smoking.
authors.affiliation: Department of Dermatology, Turku University Hospital, University of Turku, Turku, Finland.
authors.forename: P
authors.initials: P
authors.lastname: Linnamaa
authors.forename: K
authors.initials: K
authors.lastname: Nieminen
authors.forename: L
authors.initials: L
authors.lastname: Koulu
authors.forename: S
authors.initials: S
authors.lastname: Tuomasjukka
authors.forename: H
authors.initials: H
authors.lastname: Kallio
authors.forename: B
authors.initials: B
authors.lastname: Yang
authors.forename: R
authors.initials: R
authors.lastname: Tahvonen
authors.forename: J
authors.initials: J
authors.lastname: Savolainen
mesh_terms: D000328:Adult; D016207:Cytokines / Q000096:biosynthesis* / Q000276:immunology; D003876:Dermatitis, Atopic / Q000276:immunology; D005260:Female; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000276:immunology; D007223:Infant; D007249:Inflammation / Q000276:immunology; D007963:Leukocytes, Mononuclear; D008297:Male; D010290:Parents; D012907:Smoking / Q000009:adverse effects*; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D016207:Cytokines