Evidence map›Paper›PMID 41366391›Full record

ArticleRespiratory research2025

Integrative single-cell RNA and ATAC sequencing reveals the impact of chronic cigarette smoking on lung epithelial responses to influenza and hyperoxia.

Pei-Chun Cha, Zhenyang Zou, Jessica Nouws, Reginald M Brewster, Charles S Dela Cruz, Lokesh Sharma, Xiting Yan, Maor Sauler

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Article in Respiratory research, 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

8 authors.

Pei-Chun Cha *Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, CT, USA.
Zhenyang Zou *Department of Biostatistics, Yale School of Public Health, New Haven, CT, USA.
Jessica NouwsSection of Pulmonary, Critical Care and Sleep medicine, Yale School of Medicine, 300 Cedar Street (S441 TAC), New Haven, CT, 06520-8057, USA.
Reginald M BrewsterSection of Pulmonary, Critical Care and Sleep medicine, Yale School of Medicine, 300 Cedar Street (S441 TAC), New Haven, CT, 06520-8057, USA.
Charles S Dela CruzSection of Pulmonary, Critical Care and Sleep medicine, Yale School of Medicine, 300 Cedar Street (S441 TAC), New Haven, CT, 06520-8057, USA.
Lokesh SharmaSection of Pulmonary, Critical Care and Sleep medicine, Yale School of Medicine, 300 Cedar Street (S441 TAC), New Haven, CT, 06520-8057, USA.
Xiting YanDepartment of Biostatistics, Yale School of Public Health, New Haven, CT, USA.
Maor SaulerSection of Pulmonary, Critical Care and Sleep medicine, Yale School of Medicine, 300 Cedar Street (S441 TAC), New Haven, CT, 06520-8057, USA. maor.sauler@yale.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCigarette smoke (CS) increases susceptibility to acute lung injury, yet how CS reshapes epithelial responses to subsequent insults remains unclear, and the extent to which aberrant epithelial responses are linked to epigenetic changes in vivo is uncertain.

methodsIn this pilot, proof-of-principle study, we performed paired single-cell RNA-seq and ATAC-seq after chronic CS exposure followed by influenza or hyperoxia, generating joint expression–accessibility maps across epithelial subsets and inferring candidate transcriptional regulators.

resultsInfluenza and hyperoxia elicited distinct epithelial programs. Prior CS exposure amplified epigenetically regulated inflammatory signaling (cytokine/chemokine modules coupled to ERK/MAPK and PI3K) and suppressed epigenetically regulated reparative and differentiation pathways (γ-secretase/NOTCH). Transcription factor motif enrichment implicated ETS family factors and REL as candidate regulators of the CS-augmented responses in AT2 and ciliated cells.

conclusionsPaired single-cell RNA/ATAC profiling captures injury-conditioned epithelial programs and their epigenetic context after chronic CS exposure, demonstrating feasibility and providing a framework to prioritize targets of exposure-related aberrant responses.

Indexed as

Cigarette SmokingHyperoxiaLungSingle-Cell AnalysisAnimalsHumansMicePilot ProjectsSequence Analysis, RNASingle-Cell Gene Expression AnalysisEnrichment analysisHyperoxiaInfluenzaLung epitheliumScATAC-seqScRNA-seqSmoking

Identifiers

PMID41366391
PMCPMC12801856

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.