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Cigarette smoke suppresses Th1 cytokine production and increases RSV expression in a neonatal model

Respiratory Immunology and Asthma Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico

Submitted 4 April 2005 ; accepted in final form 23 August 2005

Respiratory syncytial virus (RSV) infects 90% of young children by the age of 2 yr, with peak rates occurring during 2–6 mo of age. Exposure to side-stream cigarette smoke (SS) may increase the incidence or manifestation of an RSV infection. We hypothesized that exposure to SS would alter the subsequent immune response to RSV infection in neonatal mice. BALB/c mice were exposed to air or 1.5 mg/m³ of SS from day (d) 1 up to 35 d of age. A subset was intranasally infected with 4 x 10⁴ PFU of RSV/g body wt on d 7 and rechallenged at 28 d of age. Immune responses were assessed on d 4 and 7 after RSV rechallenge. Both air- and SS-exposed mice responded to RSV rechallenge with neutrophilia and decreased Clara cell secretory protein levels within the lung. However, an increase in bronchoalveolar lavage fluid eosinophils, in addition to reduced levels of Th1 cytokines (IFN- and IL-12), decreased lung tissue inflammation, and decreased mucus production was observed in SS-exposed mice compared with air-exposed mice after RSV rechallenge. Ultimately changes in cytokine and inflammatory responses due to SS exposure likely contributed to increased viral gene expression. These results suggest that SS exposure plays a significant role in shaping the neonatal response to RSV infection.

epithelium; development; immune; lung; respiratory syncytial virus; side stream

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