Pro-inflammatory and Th2-type cytokine responses in PBMC in infants are associated with parental smoking

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.

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.

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.

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.

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.