Evidence map›Paper›PMID 33986144›Full record

ReviewThorax2022

Cigarette smoke exposure and alveolar macrophages: mechanisms for lung disease.

Sebastian T Lugg, Aaron Scott, Dhruv Parekh, Babu Naidu, David R Thickett

Open access · bronzeAbstract readReview
In one paragraph

Review in Thorax, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 197 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
197citing papers in PubMed, 4 pooled it
20.9field-weighted citation impact, top 1% of its field
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

197 citing papers in PubMed, 4 syntheses or guidelines pooled it, 366 citations in OpenAlex.

  1. Pooled it
  2. Respiratory disease in people with major depressive disorder: A systematic review and Meta-analysis.European psychiatry : the journal of the Association of European Psychiatrists · 2025
    Pooled it
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  15. Trained immunity in respiratory diseases: Mechanisms of action and intervention strategies.Chinese medical journal pulmonary and critical care medicine · 2026
    Review
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137 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Sebastian T LuggBirmingham Acute Care Research Group, Institute of Inflammation and Ageing, University of Birmingham, Birmingham, UK.
Aaron ScottBirmingham Acute Care Research Group, Institute of Inflammation and Ageing, University of Birmingham, Birmingham, UK.ORCID 0000-0001-9325-5026
Dhruv ParekhBirmingham Acute Care Research Group, Institute of Inflammation and Ageing, University of Birmingham, Birmingham, UK.
Babu NaiduBirmingham Acute Care Research Group, Institute of Inflammation and Ageing, University of Birmingham, Birmingham, UK.
David R ThickettBirmingham Acute Care Research Group, Institute of Inflammation and Ageing, University of Birmingham, Birmingham, UK d.thickett@bham.ac.uk.
University of Birmingham · GB

Funding

Medical Research Council MR/L002736/1Medical Research Council MR/S002782/1
6 · The paper itself

Abstract

Cigarette smoking is the leading cause of preventable death worldwide. It causes chronic lung disease and predisposes individuals to acute lung injury and pulmonary infection. Alveolar macrophages are sentinel cells strategically positioned in the interface between the airway lumen and the alveolar spaces. These are the most abundant immune cells and are the first line of defence against inhaled particulates and pathogens. Recently, there has been a better understanding about the ontogeny, phenotype and function of alveolar macrophages and their role, not only in phagocytosis, but also in initiating and resolving immune response. Many of the functions of the alveolar macrophage have been shown to be dysregulated following exposure to cigarette smoke. While the mechanisms for these changes remain poorly understood, they are important in the understanding of cigarette smoking-induced lung disease. We review the mechanisms by which smoking influences alveolar macrophage: (1) recruitment, (2) phenotype, (3) immune function (bacterial killing, phagocytosis, proteinase/anti-proteinase release and reactive oxygen species production) and (4) homeostasis (surfactant/lipid processing, iron homeostasis and efferocytosis). Further understanding of the mechanisms of cigarette smoking on alveolar macrophages and other lung monocyte/macrophage populations may allow novel ways of restoring cellular function in those patients who have stopped smoking in order to reduce the risk of subsequent infection or further lung injury.

Indexed as

Macrophages, AlveolarPneumoniaHumansLungPhagocytosisSmokeSmokingSmokeemphysemalung proteasesmacrophage biologyoxidative stressrespiratory infectionsurfactant proteintobacco and the lung

Identifiers

PMID33986144
PMCPMC8685655
OpenAlexW3162958603

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.