Evidence map›Paper›PMID 29543040›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2018

Cigarette smoke exposure worsens acute lung injury in antibiotic-treated bacterial pneumonia in mice.

Jeffrey E Gotts, Lauren Chun, Jason Abbott, Xiaohui Fang, Naoki Takasaka, Stephen L Nishimura, Matthew L Springer, Suzaynn F Schick, Carolyn S Calfee, Michael A Matthay

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  3. Comparable Impairment of Vascular Endothelial Function by a Wide Range of Electronic Nicotine Delivery Devices.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2022
    Article
  4. Aerosolized vitamin E acetate causes oxidative injury in mice and in alveolar macrophages.American journal of physiology. Lung cellular and molecular physiology · 2022
    Article
  5. Article
  6. Article
  7. CIGARETTE SMOKING INCREASES THE RISK OF ACUTE RESPIRATORY DISTRESS SYNDROME.Transactions of the American Clinical and Climatological Association · 2022
    Article
  8. Article
  9. Environmental Factors.Critical care clinics · 2021
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. The ex vivo perfused human lung is resistant to injury by high-doseAmerican journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  15. Clinically relevant model of pneumococcal pneumonia, ARDS, and nonpulmonary organ dysfunction in mice.American journal of physiology. Lung cellular and molecular physiology · 2019
    Article
  16. American journal of physiology. Lung cellular and molecular physiology · 2019
    Article
  17. 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

10 authors at 1 institution in 1 country.

Jeffrey E GottsDepartments of Medicine and Anesthesia, Cardiovascular Research Institute, University of California , San Francisco, California.
Lauren ChunDepartments of Medicine and Anesthesia, Cardiovascular Research Institute, University of California , San Francisco, California.
Jason AbbottDepartments of Medicine and Anesthesia, Cardiovascular Research Institute, University of California , San Francisco, California.
Xiaohui FangDepartments of Medicine and Anesthesia, Cardiovascular Research Institute, University of California , San Francisco, California.
Naoki TakasakaDepartment of Pathology, University of California , San Francisco, California.
Stephen L NishimuraDepartment of Pathology, University of California , San Francisco, California.
Matthew L SpringerDepartment of Medicine, Cardiovascular Research Institute, University of California , San Francisco, California.
Suzaynn F SchickDepartment of Medicine, Cardiovascular Research Institute, University of California , San Francisco, California.
Carolyn S CalfeeDepartments of Medicine and Anesthesia, Cardiovascular Research Institute, University of California , San Francisco, California.
Michael A MatthayDepartments of Medicine and Anesthesia, Cardiovascular Research Institute, University of California , San Francisco, California.
University of California, San Francisco · US

Funding

Training and Education p489-500P50CA180890 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GLANTZ, STANTON ARNOLD · 2013 to 2018
$20.5M
NCI NIH HHS P50 CA180890
6 · The paper itself

Abstract

Evidence is accumulating that exposure to cigarette smoke (CS) increases the risk of developing acute respiratory distress syndrome (ARDS). Streptococcus pneumoniae is the most common cause of bacterial pneumonia, which in turn is the leading cause of ARDS. Chronic smokers have increased rates of pneumococcal colonization and develop more severe pneumococcal pneumonia than nonsmokers; yet mechanistic connections between CS exposure, bacterial pneumonia, and ARDS pathogenesis remain relatively unexplored. We exposed mice to 3 wk of moderate whole body CS or air, followed by intranasal inoculation with an invasive serotype of S. pneumoniae. CS exposure alone caused no detectable lung injury or bronchoalveolar lavage (BAL) inflammation. During pneumococcal infection, CS-exposed mice had greater survival than air-exposed mice, in association with reduced systemic spread of bacteria from the lungs. However, when mice were treated with antibiotics after infection to improve clinical relevance, the survival benefit was lost, and CS-exposed mice had more pulmonary edema, increased numbers of BAL monocytes, and elevated monocyte and lymphocyte chemokines. CS-exposed antibiotic-treated mice also had higher serum surfactant protein D and angiopoietin-2, consistent with more severe lung epithelial and endothelial injury. The results indicate that acute CS exposure enhances the recruitment of immune cells to the lung during bacterial pneumonia, an effect that may provide microbiological benefit but simultaneously exposes the mice to more severe inflammatory lung injury. The inclusion of antibiotic treatment in preclinical studies of acute lung injury in bacterial pneumonia may enhance clinical relevance, particularly for future studies of current or emerging tobacco products.

Indexed as

Acute Lung InjuryPneumonia, BacterialPneumonia, PneumococcalAnimalsAnti-Bacterial AgentsFemaleMicePulmonary EdemaStreptococcus pneumoniaeTobacco Smoke PollutionAnti-Bacterial AgentsTobacco Smoke Pollutionacute lung injuryARDScigarette smokepneumococcuspneumonia

Identifiers

PMID29543040
PMCPMC6087899
OpenAlexW2790132064

What OpenQuestion holds

Textmetadata
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.