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Updated: Mar 17, 2026
A Non-invasive and Technically Non-intensive Method for Induction and Phenotyping of Experimental Bacterial Pneumonia in Mice
Published on: September 28, 2016
Cigarette smoke causes acute airway disease and exacerbates chronic obstructive lung disease in neonatal mice
Jie Jia1, Thomas M Conlon1, Carolina Ballester Lopez1
1Comprehensive Pneumology Center (CPC), Institute of Lung Biology and Disease, Helmholtz Zentrum München, Member of the German Center for Lung Research (DZL), Munich, Germany;
Insights
Neonatal exposure to cigarette smoke (CS) causes airway disease and remodeling in mice. CS worsens lung inflammation and mucus in mice with existing lung conditions, suggesting similar risks for children.
Area of Science:
- Pulmonary Medicine
- Environmental Health
- Pediatric Respiratory Research
Background:
- Postnatal cigarette smoke (CS) exposure is linked to childhood respiratory issues.
- Mechanisms of CS-induced early-onset airway disease and gene interactions are unclear.
Purpose of the Study:
- To investigate the effects of acute CS exposure on neonatal wild-type and beta-epithelial sodium ion channel (β-ENaC)-transgenic mice.
- To understand how CS exposure impacts lung inflammation, airway remodeling, and mucus production in neonatal mice with and without pre-existing lung disease.
Main Methods:
- Neonatal wild-type and β-ENaC-transgenic mice were exposed to CS for 4 days.
- Bronchoalveolar lavage fluid (BALF) analysis assessed inflammatory cell counts and protein levels (Mmp12, Cxcl1).
- Lung sections were analyzed for epithelial and vascular remodeling, mucus accumulation, goblet cell hyperplasia, and Muc5ac expression.
Main Results:
- CS exposure increased macrophages and neutrophils in wild-type mice BALF, with elevated Mmp12 and Cxcl1.
- β-ENaC-transgenic mice showed increased macrophages and significant airway neutrophilia post-CS exposure.
- CS induced airway epithelial/vascular remodeling in both mouse types, with exacerbated mucus hypersecretion and plugging in β-ENaC-transgenic mice.
Conclusions:
- Short-term CS exposure causes acute airway disease and remodeling in neonatal mice.
- CS exposure aggravates lung inflammation and mucus plugging in neonatal mice with underlying lung disease.
- Neonatal mice are susceptible to CS-induced airway disease, with risks amplified in those with chronic lung conditions.
Abstract:
Epidemiological evidence demonstrates a strong link between postnatal cigarette smoke (CS) exposure and increased respiratory morbidity in young children. However, how CS induces early onset airway disease in young children, and how it interacts with endogenous risk factors, remains poorly understood. We, therefore, exposed 10-day-old neonatal wild-type and β-epithelial sodium ion channel (β-ENaC)-transgenic mice with cystic fibrosis-like lung disease to CS for 4 days. Neonatal wild-type mice exposed to CS demonstrated increased numbers of macrophages and neutrophils in the bronchoalveolar lavage fluid (BALF), which was accompanied by increased levels of Mmp12 and Cxcl1 BALF from β-ENaC-transgenic mice contained greater numbers of macrophages, which did not increase following acute CS exposure; however, there was significant increase in airway neutrophilia compared with filtered air transgenic and CS-exposed wild-type controls. Interestingly, wild-type and β-ENaC-transgenic mice demonstrated epithelial airway and vascular remodeling following CS exposure. Morphometric analysis of lung sections revealed that CS exposure caused increased mucus accumulation in the airway lumen of neonatal β-ENaC-transgenic mice compared with wild-type controls, which was accompanied by an increase in the number of goblet cells and Muc5ac upregulation. We conclude that short-term CS exposure 1) induces acute airway disease with airway epithelial and vascular remodeling in neonatal wild-type mice; and 2) exacerbates airway inflammation, mucus hypersecretion, and mucus plugging in neonatal β-ENaC-transgenic mice with chronic lung disease. Our results in neonatal mice suggest that young children may be highly susceptible to develop airway disease in response to tobacco smoke exposure, and that adverse effects may be aggravated in children with underlying chronic lung diseases.
