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

Am J Physiol Lung Cell Mol Physiol. 2006 Feb;290(2):L222-31. doi: 10.1152/ajplung.00148.2005. Epub 2005 Aug 26.

Abstract

Respiratory syncytial virus (RSV) infects approximately 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 4x10(4) 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-gamma 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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Cytokines / biosynthesis*
  • Disease Models, Animal
  • Female
  • Inflammation Mediators / metabolism
  • Interleukins / biosynthesis
  • Lung / immunology
  • Lung / physiopathology
  • Mice
  • Mice, Inbred BALB C
  • Mucus / physiology
  • Nicotiana / adverse effects
  • Pneumonia / chemically induced
  • Pneumonia / pathology
  • Respiratory Syncytial Virus Infections / physiopathology
  • Respiratory Syncytial Viruses / metabolism
  • Smoke / adverse effects*
  • Th1 Cells / drug effects
  • Th1 Cells / metabolism
  • Uteroglobin / biosynthesis
  • Viral Proteins / biosynthesis

Substances

  • Cytokines
  • Inflammation Mediators
  • Interleukins
  • Scgb1a1 protein, mouse
  • Smoke
  • Viral Proteins
  • Uteroglobin