Background Cigarette smoke leads to pulmonary inflammatory injury. Relevant studies confirm it also disturbs gut microbiota and metabolism, but few time-course experiments are performed on juvenile rats. This study investigated intestinal microbial and metabolic alterations under CSE-induced lung injury. Methods Male Wistar rats were randomly assigned to 3 groups: Control, 4-week CSE exposure (CSE 4 W), and 8-week CSE exposure (CSE 8 W). A modified intranasal instillation method was used to establish a lung injury model. Pulmonary function tests and histopathological evaluations were conducted to verify model establishment. Fecal samples were collected for 16S rRNA sequencing to profile the gut microbiota and for gas chromatography–mass spectrometry (GC-MS) to quantify SCFAs levels. Results Compared with the Control group, CSE 8 W group exhibited significantly impaired pulmonary function and elevated histopathological scores. Both α- and β-diversity of the gut microbiota were markedly altered. Concurrently, fecal concentrations of butyric acid and caproic acid were significantly decreased in the CSE 8 W group. Conclusion CSE exposure induces progressive gut microbial dysbiosis and perturbs SCFA metabolism in juvenile rats. These findings provide experimental evidence linking CSE-exposure to intestinal alterations, suggesting further investigation into the potential mechanisms. Impact <UnorderedList Mark="Bullet"> <ItemContent> CSE exposure in juvenile rats causes progressive lung injury, time-dependent gut dysbiosis, and disrupted SCFA metabolism, simulating smoking’s harm to children’s gut homeostasis. </ItemContent> <ItemContent> It links pulmonary damage to declines in beneficial SCFA producers (e.g., Blautia) and reduced SCFA via systematic time-course analysis. </ItemContent> <ItemContent> Lung-derived inflammation may disrupt gut homeostasis, reduce beneficial SCFA production, and form a vicious cycle. </ItemContent> <ItemContent> It underscores the need for understanding the crosstalk between CSE-exposed lungs and intestinal injury, identifying specific taxa and metabolites as potential biomarkers or intervention targets for pediatric tobacco harm mitigation. </ItemContent> </UnorderedList>

Cigarette smoke extract exposure induces gut microbial dysbiosis and impairs short-chain fatty acid metabolism in juvenile rats

期刊论文
发表日期：

2026年7月28日

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Jingjing Wei,
Chunli Xu,
Quan Yun,
Meiqi Guan,
Jianing Xie,
Yuan Tian,
Guoquan Fan

摘要

Background

Cigarette smoke leads to pulmonary inflammatory injury. Relevant studies confirm it also disturbs gut microbiota and metabolism, but few time-course experiments are performed on juvenile rats. This study investigated intestinal microbial and metabolic alterations under CSE-induced lung injury.

Methods

Male Wistar rats were randomly assigned to 3 groups: Control, 4-week CSE exposure (CSE 4 W), and 8-week CSE exposure (CSE 8 W). A modified intranasal instillation method was used to establish a lung injury model. Pulmonary function tests and histopathological evaluations were conducted to verify model establishment. Fecal samples were collected for 16S rRNA sequencing to profile the gut microbiota and for gas chromatography–mass spectrometry (GC-MS) to quantify SCFAs levels.

Results

Compared with the Control group, CSE 8 W group exhibited significantly impaired pulmonary function and elevated histopathological scores. Both α- and β-diversity of the gut microbiota were markedly altered. Concurrently, fecal concentrations of butyric acid and caproic acid were significantly decreased in the CSE 8 W group.

Conclusion

CSE exposure induces progressive gut microbial dysbiosis and perturbs SCFA metabolism in juvenile rats. These findings provide experimental evidence linking CSE-exposure to intestinal alterations, suggesting further investigation into the potential mechanisms.

Impact

CSE exposure in juvenile rats causes progressive lung injury, time-dependent gut dysbiosis, and disrupted SCFA metabolism, simulating smoking’s harm to children’s gut homeostasis.

It links pulmonary damage to declines in beneficial SCFA producers (e.g., Blautia) and reduced SCFA via systematic time-course analysis.

Lung-derived inflammation may disrupt gut homeostasis, reduce beneficial SCFA production, and form a vicious cycle.

It underscores the need for understanding the crosstalk between CSE-exposed lungs and intestinal injury, identifying specific taxa and metabolites as potential biomarkers or intervention targets for pediatric tobacco harm mitigation.