Evidence map›Paper›PMID 17056580›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2006

Decreased alveolar macrophage apoptosis is associated with increased pulmonary inflammation in a murine model of pneumococcal pneumonia.

Helen M Marriott, Paul G Hellewell, Simon S Cross, Paul G Ince, Moira K B Whyte, David H Dockrell

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 94 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Contribution of Puma to Inflammatory Resolution During Early Pneumococcal Pneumonia.Frontiers in cellular and infection microbiology · 2022
    Article
  6. Article
  7. Therapeutic options of TCM for organ injuries associated with COVID-19 and the underlying mechanism.Phytomedicine : international journal of phytotherapy and phytopharmacology · 2021
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
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  15. Article
  16. Article
  17. Review
  18. Article
  19. Diverse macrophage populations mediate acute lung inflammation and resolution.American journal of physiology. Lung cellular and molecular physiology · 2014
    Review
  20. 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

6 authors at 1 institution in 1 country.

Helen M MarriottSchool of Medicine and Biomedical Sciences, University of Sheffield, Beech Hill Road, Sheffield S10 2RX, United Kingdom.
Paul G Hellewell
Simon S Cross
Paul G Ince
Moira K B Whyte
David H Dockrell
University of Sheffield · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulation of the inflammatory infiltrate is critical to the successful outcome of pneumonia. Alveolar macrophage apoptosis is a feature of pneumococcal infection and aids disease resolution. The host benefits of macrophage apoptosis during the innate response to bacterial infection are incompletely defined. Because NO is required for optimal macrophage apoptosis during pneumococcal infection, we have explored the role of macrophage apoptosis in regulating inflammatory responses during pneumococcal pneumonia, using inducible NO synthase (iNOS)-deficient mice. iNOS(-/-) mice demonstrated decreased numbers of apoptotic macrophages as compared with wild-type C57BL/6 mice following pneumococcal challenge, greater recruitment of neutrophils to the lung and enhanced expression of TNF-alpha. Pharmacologic inhibition of iNOS produced similar results. Greater pulmonary inflammation was associated with greater levels of early bacteremia, IL-6 production, lung inflammation, and mortality within the first 48 h in iNOS(-/-) mice. Labeled apoptotic alveolar macrophages were phagocytosed by resident macrophages in the lung and intratracheal instillation of exogenous apoptotic macrophages decreased neutrophil recruitment in iNOS(-/-) mice and decreased TNF-alpha mRNA in lungs and protein in bronchial alveolar lavage, as well as chemokines and cytokines including IL-6. These changes were associated with a lower probability of mice becoming bacteremic. This demonstrates the potential of apoptotic macrophages to down-regulate the inflammatory response and for the first time in vivo demonstrates that clearance of apoptotic macrophages decreases neutrophil recruitment and invasive bacterial disease during pneumonia.

Indexed as

ApoptosisAnimalsBacteremiaBiomarkersDisease Models, AnimalLungMacrophages, AlveolarMiceMice, Mutant StrainsNeutrophilsNitric Oxide Synthase Type IIPneumonia, PneumococcalStreptococcus pneumoniaeTumor Necrosis Factor-alphaBiomarkersNitric Oxide Synthase Type IITumor Necrosis Factor-alpha

Identifiers

PMID17056580
PMCPMC7611733
OpenAlexW1918446975

What OpenQuestion holds

Textmetadata
LicenceTDM
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.