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Published on: January 16, 2015
Impaired lung homeostasis in neonatal mice exposed to cigarette smoke
Sharon McGrath-Morrow1, Tirumalai Rangasamy, Cecilia Cho
1Department of Pediatrics, Division of Pediatric Pulmonary, Johns Hopkins Hospital, Park 316/600 N. Wolfe St., Baltimore, MD 21287-2533, USA. smorrow@jhmi.edu
Insights
Neonatal exposure to cigarette smoke (CS) harms infant lung development. This study found CS exposure in newborn mice suppressed immune genes and impaired lung growth, potentially explaining increased respiratory issues in children.
Area of Science:
- Pulmonary Medicine
- Immunology
- Developmental Biology
Background:
- Infant smoke exposure correlates with respiratory illnesses and reduced lung function.
- The perinatal period is a critical window for lung development, potentially increasing susceptibility to environmental toxins like cigarette smoke (CS).
Purpose of the Study:
- To investigate the effects of neonatal cigarette smoke (CS) exposure on lung immunity and growth in mice.
- To determine if perinatal CS exposure alters immune gene expression and lung development.
Main Methods:
- Neonatal mice were exposed to CS for 14 days.
- Pulmonary gene expression profiling, immunohistochemistry (Nitrotyrosine, TUNEL, MAC3, p-SMAD2), and lung volume measurements were performed.
Main Results:
- CS exposure significantly inhibited type 1 and type 2 interferon pathway genes in neonatal lungs.
- Increased Nitrotyrosine, TUNEL, and p-SMAD2 staining observed in neonatal CS-exposed lungs.
- CS exposure during the neonatal period led to modestly decreased lung volumes at 8 weeks, indicating impaired lung growth.
Conclusions:
- Neonatal CS exposure suppresses innate immune gene expression in the developing lung.
- Perinatal CS exposure results in mild impairment of postnatal lung growth.
- These findings may explain the higher incidence of respiratory symptoms in infants exposed to CS.
Abstract:
In infants, smoke exposure is associated with more respiratory illnesses and decreased lung function. We hypothesized that perinatal lung is particularly susceptible to the damaging effects of cigarette smoke (CS) and that exposure to CS during this period may alter expression of immune response genes and adversely affect lung growth. To test this, we exposed neonatal mice to 14 days of CS. Immediately after exposure to CS, pulmonary gene expression profiling was performed on 2-week-old CS-exposed lung and age-matched control lung. Nitrotyrosine, TUNEL, MAC3, and phospho-SMAD-2 (p-SMAD2) staining was also performed. At 8 weeks of age, lung volume measurements were determined and mean linear intercept measurements were calculated. Pulmonary gene expression profiling revealed that CS exposure significantly inhibited type 1 and type 2 interferon pathway genes in neonatal lung, compared with age-matched control lung. Neonatal CS-exposed lung also had a significant increase in n-tyrosine, TUNEL, and p-SMAD2 staining when compared with adult CS-exposed lung and age-matched control lung. Lung volumes at 8 weeks of age were modestly but significantly decreased in mice exposed to CS in the neonatal period compared with age-matched controls, consistent with impaired lung growth. The results of this study indicate that exposure to CS during the neonatal period inhibits expression of genes involved in innate immunity and mildly impairs postnatal lung growth. These findings may in part explain the increased incidence of respiratory symptoms in infants and children exposed to CS.
