Newswise — Diminished production of dendritic cell interleukin 10 (IL-10), an anti-inflammatory cytokine previously associated with asthma, is linked to environmental tobacco smoke during infancy in a study published this month in Annals of Allergy, Asthma & Immunology, the scientific journal of the American College of Allergy, Asthma and Immunology (ACAAI).

The pilot study, conducted by Deborah Gentile, M.D., and colleagues at the Allegheny General Hospital and in part at Children's Hospital of Pittsburgh, in Pittsburgh, evaluated environmental tobacco smoke in 37 healthy infants by questionnaire and by obtaining blood samples at 2 weeks, 3 months, and 5 months of age. The infants were divided into two groups of 21 with a history of exposure to environmental tobacco smoke and 16 without.

Detectable IL-10 levels was similar in both groups at 2 weeks and 3 months, but significantly different at 5 months. In those without environmental tobacco smoke exposure, the IL-10 levels increased during the observation period by 25 percent at 2 weeks, 20 percent at 3 months, and 36 percent at 5 months. In contrast, in those with environmental tobacco smoke exposure, the frequency with detectable IL-10 levels decreased 33 percent at 2 weeks, 19 percent at 3 months and 7 percent at 5 months.

Dendritic cells are critically involved in the initiation of primary immune processes, and IL-10 plays a key regulatory role in allergic diseases.

Dr. Gentile and her team conclude that future studies need to expand the sample sizes and explore whether diminished dendritic cell IL-10 production is the mechanism by which environmental tobacco smoke predisposes patients to the development of asthma and/or atopy.

The ACAAI is a professional medical organization comprising 4,963 qualified allergists-immunologists and related health care professionals. The College is dedicated to the clinical practice of allergy, asthma and immunology through education and research to promote the highest quality of patient care.

Ann Allergy Asthma Immunol. April 2004; 92:433-437

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CITATIONS

Annals of Allergy, Asthma & Immunology, April 2004 (Apr-2004)