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Parental tobacco smoking is associated with augmented IL-13 secretion in children with allergic asthma.
Feleszko, Wojciech MD, PhD a,*; Zawadzka-Krajewska, Anna MD, PhD a; Matysiak, Katarzyna MD b; Lewandowska, Dorota MD b; Peradzynska, Joanna MD a; Dinh, Q. Thai MD, PhD c; Hamelmann, Eckard MD, PhD d; Groneberg, David A. MD, PhD c; Kulus, Marek MD, PhD a
[Article] Journal of Allergy & Clinical Immunology. 117(1):97-102, January 2006.

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Background: Exposure to environmental tobacco smoke (ETS) has been shown to increase symptoms of allergic bronchial asthma, but direct effects on the expression of inflammatory markers have not been demonstrated thus far.

Objective: The aim of this study was to assess the correlation of ETS exposure with the expression of proinflammatory mediators in airway secretions, including IFN-[gamma] and IL-12, as well as IL-5 and IL-13, in allergic asthmatic schoolchildren and healthy control subjects.

Methods: By using the nasopharyngeal aspiration technique, airway secretions were collected from 24 atopic children with asthma (age, 6-16 years) and 26 healthy control subjects, and the concentration of cytokines was measured with immunoenzymatic methods.

Results: IL-13 levels were highly increased in patients with asthma (P < .005), and parental tobacco smoke resulted in a significant increase in airway IL-13 secretion in these children compared with that seen in nonexposed children and healthy control subjects (median, 860 pg/mL vs 242 pg/mL and 125 pg/mL, respectively). Furthermore, a positive correlation between IL-13 levels and serum IgE concentrations (rs = 0.55) was found in children with allergic asthma.

Conclusions: These results indicate that ETS augments the expression and secretion of IL-13 in allergic asthma and that nasopharyngeal aspiration is a suitable method to assess cytokine measurements in airways in children. Measurements of IL-13 in secretions might be taken into account as a noninvasive marker of airway inflammation and to assess the detrimental effects of ETS.