Evidence map›Paper›PMID 40969777›Full record

ArticleTobacco induced diseases2025

Mouse model validity for studying the impact of tobacco smoke on the human gut microbiota assessed via in silico and experimental approaches.

Irene Victoria Bermúdez-Pérez, Juliana Meißner, Corinna Bang, Jan N Hartmann, John F Baines, Susanne Krauss-Etschmann, Robert Häsler

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Article in Tobacco induced diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Irene Victoria Bermúdez-Pérez *Department of Dermatology and Allergy, University Hospital Schleswig-Holstein, Kiel, Germany.
Juliana Meißner *Division of Early Life Origins of Chronic Lung Diseases, Research Center Borstel, Airway Research Center North, German Center for Lung Research, Borstel, Germany.
Corinna BangInstitute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, Kiel, Germany.
Jan N HartmannDepartment of Dermatology and Allergy, University Hospital Schleswig-Holstein, Kiel, Germany.
John F BainesSection of Evolutionary Medicine, Max Planck Institute for Evolutionary Biology, Plön, Germany.
Susanne Krauss-EtschmannDivision of Early Life Origins of Chronic Lung Diseases, Research Center Borstel, Airway Research Center North, German Center for Lung Research, Borstel, Germany.
Robert HäslerDepartment of Dermatology and Allergy, University Hospital Schleswig-Holstein, Kiel, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe contribution of cigarettes to disease initiation, manifestation and progression is well-established for complex disorders, such as inflammatory bowel disease. However, studying its impact on disease pathophysiology in a controlled setting is challenging in humans, resulting in the application of various model systems, amongst them tobacco smoke-exposed mice. While frequently employed, it is unclear to what extent this model reflects human responses to tobacco smoke.

methodsEmploying a mouse study of experimental nature, we assessed established parameters for monitoring responses to tobacco smoke, paralleled by 16S rRNA gene-based profiling of the murine gut microbiome in n=32 suitable animals. This was supplemented by a case-control study design, based on n=3 publicly available transcriptome datasets, from human oral mucosa, human large airway epithelium and murine lung tissues, where we assessed which components of the response to tobacco smoke observed in mice are functionally comparable to responses seen in humans.

resultsWe observed several physiological responses in mice that paralleled human scenarios (weight loss, serum cotinine and Cyp1a1 mRNA expression), serving as a proof of principle. We identified shared microbiome-associated processes: stress related functions were enriched in mice and humans, while other processes, such as inflammatory functions, were discordant. The mouse microbiota showed significant changes in response to tobacco smoke, which mimicked patterns seen in human datasets, such as changes for

conclusionsConsidering the high inter-individual variation in humans and the well-controlled conditions in mice, our results suggest that mice, despite the identified limitations, most likely represent a suitable model for studying specific processes, such as stress responses, in the context of tobacco smoke exposure and its impact on the microbiota.

Indexed as

microbiotamouse modelsequencingsmokingtranscriptome

Identifiers

PMID40969777
PMCPMC12442884

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