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Cigarette smoke suppresses Th1 cytokine production and increases RSV expression in a neonatal model
Vatsana Phaybouth1, Shan-Ze Wang, Julie A Hutt
1Respiratory Immunology and Asthma Program, Lovelace Respiratory Research Inst., 2425 Ridgecrest Dr. SE, Albuquerque, NM 87108, USA.
Insights
Exposure to secondhand smoke (SS) in neonatal mice alters immune responses to respiratory syncytial virus (RSV) infection. SS-exposed mice showed increased eosinophils and reduced Th1 cytokines, potentially worsening RSV outcomes.
Area of Science:
- Immunology
- Environmental Health
- Pediatrics
Background:
- Respiratory syncytial virus (RSV) is a common childhood infection, particularly in infants.
- Exposure to secondhand smoke (SS) is a potential environmental risk factor for increased severity of RSV infections.
Purpose of the Study:
- To investigate the impact of neonatal SS exposure on the immune response to subsequent RSV infection in a mouse model.
Main Methods:
- Neonatal BALB/c mice were exposed to air or SS (1.5 mg/m3) from day 1 to 35.
- Mice were infected with RSV on day 7 and rechallenged on day 28.
- Immune responses, including cellular and cytokine profiles in bronchoalveolar lavage fluid and lung tissue, were assessed post-rechallenge.
Main Results:
- SS-exposed mice exhibited increased eosinophils in bronchoalveolar lavage fluid post-RSV rechallenge.
- Reduced levels of Th1 cytokines (IFN-gamma, IL-12), decreased lung inflammation, and diminished mucus production were observed in SS-exposed mice.
- SS exposure was associated with increased viral gene expression, suggesting a compromised immune response.
Conclusions:
- Neonatal exposure to SS significantly alters the immune response to RSV infection.
- These alterations, including a shift towards eosinophilic inflammation and reduced Th1 responses, may contribute to increased viral replication and disease severity.
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.
