ORIGINAL RESEARCH article
Front. Immunol.
Sec. Inflammation
Concentration-dependent effects of tobacco smoke on airway inflammation and remodeling in asthmatic models
Provisionally accepted
- Deyang People's Hospital, Deyang, China
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Objective: This study aimed to investigate the effects of different concentrations of tobacco smoke on airway remodeling and airway inflammation in mouse models of asthma with distinct inflammatory phenotypes. Methods: Asthmatic mouse models were established, including an eosinophilic asthma (EA) model via ovalbumin (OVA) sensitization/challenge, a neutrophilic asthma (NA) model via OVA combined with lipopolysaccharide (LPS, 10μg) sensitization/challenge, and a mixed granulocytic asthma (MGA) model via OVA combined with LPS (0.1μg) sensitization/challenge. These mice were then exposed to tobacco environments at concentrations of 100 mg/m³ and 800 mg/m³. Body weight changes and clinical symptoms were observed and recorded. Levels of inflammatory factors (TNF-α, IFN-γ, IL-6, IL-12, MCP-1, and IL-10) in bronchoalveolar lavage fluid (BALF) were measured by ELISA. Lung histopathological changes were assessed via hematoxylin and eosin (HE) staining, while bronchial goblet cell hyperplasia and mucus secretion were observed using periodic acid-Schiff (PAS) staining. Pulmonary fibrosis was assessed using Masson's trichrome staining. Result: Compared with the blank control group, mice in the EA, NA, and MGA model groups showed significantly reduced body weight growth rate (P < 0.001) and aggravated respiratory symptoms. Tobacco smoke exposure further exacerbated these symptoms in a concentration-dependent manner. Regarding inflammatory factors, the levels of pro-inflammatory factors (TNF-α, IFN-γ, IL-6, MCP-1, IL-12) in BALF were significantly elevated, while the level of the anti-inflammatory factor IL-10 was significantly decreased (P < 0.001) in the EA, NA, and MGA model groups. Tobacco smoke exposure significantly aggravated the airway inflammatory response in these different asthmatic models in a concentration-dependent manner (P < 0.001). HE staining results demonstrated that tobacco smoke exposure worsened pathological injuries in the lung tissues of the different asthmatic models, including alveolar collapse, inflammatory cell infiltration, and epithelial cell necrosis, with the most severe damage observed in the 800 mg/m³ exposure group. PAS staining results revealed a significant increase in the percentage of goblet cells in the lung tissues of the different asthmatic models exposed to 800 mg/m³ tobacco smoke (P < 0.01, P < 0.05, and P < 0.01, respectively).
Keywords: airway inflammation, Airway Remodeling, Asthma, Inflammatory factors, Tobacco smoke
Received: 25 Dec 2025; Accepted: 10 Feb 2026.
Copyright: © 2026 Peng, Tong, Yue, Li, Han, Zeng and Feng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Feng Tong
Yinhe Feng
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