Evidence map›Paper›PMID 39182076›Full record

ArticleRespiratory research2024

Transcriptomic analysis reveals distinct effects of cigarette smoke on murine airspace and bone-marrow derived macrophages.

Lynne Faherty, William Z Zhang, Mays M Salih, Elektra K Robinson, Elizabeth Perez, Kihwan Kim, Susan Carpenter, Suzanne M Cloonan

Abstract readLetter
In one paragraph

Article in Respiratory research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Lynne Faherty *School of Medicine, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland.
William Z Zhang *Division of Pulmonary and Critical Care Medicine, Joan and Sanford I. Weill Department of Medicine, New York, NY, USA.
Mays M SalihDepartment of Molecular, Cell and Developmental Biology, University of California Santa Cruz, Santa Cruz, CA, USA.
Elektra K RobinsonDepartment of Molecular, Cell and Developmental Biology, University of California Santa Cruz, Santa Cruz, CA, USA.
Elizabeth PerezDivision of Pulmonary and Critical Care Medicine, Joan and Sanford I. Weill Department of Medicine, New York, NY, USA.
Kihwan KimDivision of Pulmonary and Critical Care Medicine, Joan and Sanford I. Weill Department of Medicine, New York, NY, USA.
Susan CarpenterDepartment of Molecular, Cell and Developmental Biology, University of California Santa Cruz, Santa Cruz, CA, USA.
Suzanne M CloonanSchool of Medicine, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland. suzanne.cloonan@tcd.ie.

Funding

Alveolar Macrophage Iron Overload in COPD PathogenesisK08HL165081 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI WILLIAM ZHENGYANG ZHANG · 2023 to 2026
$676k
NHLBI NIH HHS K08 HL165081
6 · The paper itself

Abstract

backgroundChronic obstructive pulmonary disease (COPD) is an inflammatory airway disease characterized by emphysema and chronic bronchitis and a leading cause of mortality worldwide. COPD is commonly associated with several comorbid diseases which contribute to exacerbated patient outcomes. Cigarette smoke (CS) is the most prominent risk factor for COPD development and progression and is known to be detrimental to numerous effector functions of lung resident immune cells, including phagocytosis and cytokine production. However, how CS mediates the various pathologies distant from the lung in COPD, and whether CS has a similar biological effect on systemic immune cells remains unknown.

methodsC57BL/6 mice were exposed to 8 weeks of CS as an experimental model of COPD. Bone marrow cells were isolated from both CS-exposed and room air (RA) control mice and differentiated to bone marrow-derived macrophages (BMDMs). Airspace macrophages (AMs) were isolated from the same CS-exposed and RA mice and bulk RNA-Seq performed. The functional role of differentially expressed genes was assessed through gene ontology analyses. Ingenuity Pathway Analysis was used to determine the activation states of canonical pathways and upstream regulators enriched in differentially expressed genes in both cell types, and to compare the differences between the two cell types.

resultsCS induced transcriptomic changes in BMDMs, including an upregulation of genes in sirtuin signalling and oxidative phosphorylation pathways and a downregulation of genes involved in histone and lysine methylation. In contrast, CS induced decreased expression of genes involved in pathogen response, phagosome formation, and immune cell trafficking in AMs. Little overlap was observed in differentially expressed protein-coding genes in BMDMs compared to AMs and their associated pathways, highlighting the distinct effects of CS on immune cells in different compartments.

conclusionsCS exposure can induce transcriptomic remodelling in BMDMs which is distinct to that of AMs. Our study highlights the ability of CS exposure to affect immune cell populations distal to the lung and warrants further investigation into the functional effects of these changes and the ensuing role in driving multimorbid disease.

Indexed as

Gene Expression ProfilingMice, Inbred C57BLAnimalsCells, CulturedMacrophagesMacrophages, AlveolarMaleMicePulmonary Disease, Chronic ObstructiveSmokeTranscriptomeSmokeCigarette smokeCOPDMacrophageTranscriptome

Identifiers

PMID39182076
PMCPMC11344945

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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.