Evidence map›Paper›PMID 24945405›Full record

ArticlePLoS pathogens2014

The triggering receptor expressed on myeloid cells 2 inhibits complement component 1q effector mechanisms and exerts detrimental effects during pneumococcal pneumonia.

Omar Sharif, Riem Gawish, Joanna M Warszawska, Rui Martins, Karin Lakovits, Anastasiya Hladik, Bianca Doninger, Julia Brunner, Ana Korosec, Roland E Schwarzenbacher and 9 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

42 citing papers in PubMed, 58 citations in OpenAlex.

  1. Monocytes in pneumonia: Functional plasticity and innate memory (Review).International journal of molecular medicine · 2026
    Review
  2. Article
  3. TREM2 drives monocyte-derived macrophage responses tobioRxiv : the preprint server for biology · 2026
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  19. CXCR4eLife · 2022
    Article
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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

19 authors at 6 institutions in 4 countries.

Omar SharifCeMM - Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria; Department of Medicine I, Laboratory of Infection Biology, Medical University of Vienna, Vienna, Austria.
Riem GawishCeMM - Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria; Department of Medicine I, Laboratory of Infection Biology, Medical University of Vienna, Vienna, Austria.
Joanna M WarszawskaCeMM - Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria; Department of Medicine I, Laboratory of Infection Biology, Medical University of Vienna, Vienna, Austria.
Rui MartinsCeMM - Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria; Department of Medicine I, Laboratory of Infection Biology, Medical University of Vienna, Vienna, Austria.
Karin LakovitsDepartment of Medicine I, Laboratory of Infection Biology, Medical University of Vienna, Vienna, Austria.
Anastasiya HladikCeMM - Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria; Department of Medicine I, Laboratory of Infection Biology, Medical University of Vienna, Vienna, Austria.
Bianca DoningerCeMM - Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria; Department of Medicine I, Laboratory of Infection Biology, Medical University of Vienna, Vienna, Austria.
Julia BrunnerCeMM - Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria; Department of Medicine I, Laboratory of Infection Biology, Medical University of Vienna, Vienna, Austria.
Ana KorosecCeMM - Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria; Department of Medicine I, Laboratory of Infection Biology, Medical University of Vienna, Vienna, Austria.
Roland E SchwarzenbacherCeMM - Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria; Department of Medicine I, Laboratory of Infection Biology, Medical University of Vienna, Vienna, Austria.
Tiina BergCeMM - Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
Robert KralovicsCeMM - Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
Jacques ColingeCeMM - Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
Ildiko MesteriDepartment of Pathology, Medical University of Vienna, Vienna, Austria.
Susan GilfillanDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Andrea SalmaggiDepartment of Clinical Neurosciences, Istituto Nazionale Neurologico Carlo Besta, Milano, Italy.
Admar VerschoorInstitute for Medical Microbiology, Immunology and Hygiene, Technical University Munich, Munich, Germany.
Marco ColonnaDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, United States of America.
Sylvia KnappCeMM - Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria; Department of Medicine I, Laboratory of Infection Biology, Medical University of Vienna, Vienna, Austria.
CeMM Research Center for Molecular Medicine · ATAustrian Academy of Sciences · ATMedical University of Vienna · ATWashington University in St. Louis · USFondazione IRCCS Istituto Neurologico Carlo Besta · ITInstitute of Medical Microbiology and Hygiene · DE

Funding

Austrian Science Fund FWF P 25801Austrian Science Fund FWF W 1205
6 · The paper itself

Abstract

Phagocytosis and inflammation within the lungs is crucial for host defense during bacterial pneumonia. Triggering receptor expressed on myeloid cells (TREM)-2 was proposed to negatively regulate TLR-mediated responses and enhance phagocytosis by macrophages, but the role of TREM-2 in respiratory tract infections is unknown. Here, we established the presence of TREM-2 on alveolar macrophages (AM) and explored the function of TREM-2 in the innate immune response to pneumococcal infection in vivo. Unexpectedly, we found Trem-2(-/-) AM to display augmented bacterial phagocytosis in vitro and in vivo compared to WT AM. Mechanistically, we detected that in the absence of TREM-2, pulmonary macrophages selectively produced elevated complement component 1q (C1q) levels. We found that these increased C1q levels depended on peroxisome proliferator-activated receptor-δ (PPAR-δ) activity and were responsible for the enhanced phagocytosis of bacteria. Upon infection with S. pneumoniae, Trem-2(-/-) mice exhibited an augmented bacterial clearance from lungs, decreased bacteremia and improved survival compared to their WT counterparts. This work is the first to disclose a role for TREM-2 in clinically relevant respiratory tract infections and demonstrates a previously unknown link between TREM-2 and opsonin production within the lungs.

Indexed as

Disease Models, AnimalAnimalsApoptosisCell Line, TransformedCells, CulturedComplement C1qCytokinesFemaleLungMacrophages, AlveolarMaleMembrane GlycoproteinsMice, Inbred C57BLMice, KnockoutNeutrophil InfiltrationPhagocytosisComplement C1qCytokinesMembrane GlycoproteinsPPAR gammaReceptors, ImmunologicTrem2 protein, mouse

Identifiers

PMID24945405
PMCPMC4055749
OpenAlexW1978554459

What OpenQuestion holds

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Registered trials

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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.