Evidence map›Paper›PMID 19124657›Full record

ArticleThe Journal of experimental medicine2009

Efferocytosis impairs pulmonary macrophage and lung antibacterial function via PGE2/EP2 signaling.

Alexandra I Medeiros, Carlos H Serezani, Sang Pyo Lee, Marc Peters-Golden

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

104 citing papers in PubMed, 159 citations in OpenAlex.

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  9. Molecular dynamics of inflammation resolution: therapeutic implications.Frontiers in cell and developmental biology · 2025
    Review
  10. Cellular and molecular mechanisms of skin wound healing.Nature reviews. Molecular cell biology · 2024
    Review
  11. Different bacterial cargo in apoptotic cells drive distinct macrophage phenotypes.Apoptosis : an international journal on programmed cell death · 2024
    Article
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  13. Article
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44 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

4 authors at 2 institutions in 1 country.

Alexandra I MedeirosDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Health Systems, Ann Arbor, MI 48109, USA.
Carlos H Serezani
Sang Pyo Lee
Marc Peters-Golden
Michigan Medicine · USDeleted Institution

Funding

LEUKOTRIENES AND PULMONARY ANTIBACTERIAL DEFENSER01HL058897 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PETERS-GOLDEN, MARC L · 1997 to 2012
$4.1M
Eicosanoids and lung macrophage antimicrobial mechanismsR56HL058897 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PETERS-GOLDEN, MARC L · 2008 to 2008
$383k
NHLBI NIH HHS HL058897NHLBI NIH HHS R01 HL058897NHLBI NIH HHS R56 HL058897
6 · The paper itself

Abstract

The ingestion of apoptotic cells (ACs; termed "efferocytosis") by phagocytes has been shown to trigger the release of molecules such as transforming growth factor beta, interleukin-10 (IL-10), nitric oxide, and prostaglandin E(2) (PGE(2)). Although the antiinflammatory actions of these mediators may contribute to the restoration of homeostasis after tissue injury, their potential impact on antibacterial defense is unknown. The lung is highly susceptible to diverse forms of injury, and secondary bacterial infections after injury are of enormous clinical importance. We show that ACs suppress in vitro phagocytosis and bacterial killing by alveolar macrophages and that this is mediated by a cyclooxygenase-PGE(2)-E prostanoid receptor 2 (EP2)-adenylyl cyclase-cyclic AMP pathway. Moreover, intrapulmonary administration of ACs demonstrated that PGE(2) generated during efferocytosis and acting via EP2 accounts for subsequent impairment of lung recruitment of polymorphonuclear leukocytes and clearance of Streptococcus pneumoniae, as well as enhanced generation of IL-10 in vivo. These results suggest that in addition to their beneficial homeostatic influence, antiinflammatory programs activated by efferocytosis in the lung have the undesirable potential to dampen innate antimicrobial responses. They also identify an opportunity to reduce the incidence and severity of pneumonia in the setting of lung injury by pharmacologically targeting synthesis of PGE(2) or ligation of EP2.

Indexed as

Adenylyl Cyclase InhibitorsAnimalsApoptosisCulture Media, ConditionedCyclic AMPCyclooxygenase InhibitorsDinoprostoneHumansInterleukin-10Jurkat CellsLungMacrophages, AlveolarMiceMice, Inbred C57BLMice, KnockoutNeutrophilsAdenylyl Cyclase InhibitorsCulture Media, ConditionedCyclic AMPCyclooxygenase InhibitorsDinoprostoneInterleukin-10Prostaglandin AntagonistsPTGER2 protein, humanPtger2 protein, mouseReceptors, Prostaglandin EReceptors, Prostaglandin E, EP2 Subtype

Identifiers

PMID19124657
PMCPMC2626688
OpenAlexW2081603767

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.