Evidence map›Paper›PMID 23575697›Full record

ArticleEuropean journal of immunology2013

The interaction between C5a and both C5aR and C5L2 receptors is required for production of G-CSF during acute inflammation.

Markus Bosmann, Mikel D Haggadone, Firas S Zetoune, J Vidya Sarma, Peter A Ward

Open access · greenAbstract read
In one paragraph

Article in European journal of immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.2field-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

20 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Cell-intrinsic C5a synergizes with Dectin-1 in macrophages to mediate fungal killing.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Review
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  7. T Cell Expression of C5a Receptor 2 Augments Murine Regulatory T Cell (TJournal of immunology (Baltimore, Md. : 1950) · 2018
    Article
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  20. Extracellular histones are essential effectors of C5aR- and C5L2-mediated tissue damage and inflammation in acute lung injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    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

5 authors at 1 institution in 2 countries.

Markus BosmannDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109-5602, USA.
Mikel D Haggadone
Firas S Zetoune
J Vidya Sarma
Peter A Ward
University of Michigan–Ann Arbor · US

Funding

Regulation of Lung Inflammation by Catecholamines and Adrenergic ReceptorsR01GM029507 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WARD, PETER A · 1985 to 2013
$3.9M
Protective Effects of Anti-C5a in SepsisR01GM061656 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WARD, PETER A · 2002 to 2013
$3.8M
LUNG INJURY BY OXYGEN METABOLITESR37GM029507 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WARD, PETER A · 1987 to 1996
–
NIGMS NIH HHS GM-29507NIGMS NIH HHS GM-61656NIGMS NIH HHS R01 GM029507NIGMS NIH HHS R01 GM061656NIGMS NIH HHS R37 GM029507
6 · The paper itself

Abstract

The complement activation product, C5a, is a key factor for regulation of inflammatory responses. C5a and C5adesArg bind to their receptors, C5aR and C5L2, but the functional roles of C5L2 remain controversial. We screened the patterns of 23 inflammatory mediators in cultures of LPS-activated mouse peritoneal elicited macrophages (PEMs) in the presence or absence of recombinant mouse C5a. Production of most mediators studied was suppressed by C5a, whereas G-CSF production was enhanced. G-CSF gene expression and secretion from PEMs was amplified two- to threefold by C5a in a dose- and time-dependent fashion. The degradation product C5adesArg promoted lower levels of G-CSF. The effects of C5a on G-CSF were associated with activation of PI3K/Akt and MEK1/2 signaling pathways. C5a did not enhance G-CSF production in cultures of PEMs from either C5aR- or C5L2-deficient mice, indicating that both C5a receptors are indispensable for mediating the effects of C5a in the production of G-CSF. Finally, G-CSF levels in plasma during polymicrobial sepsis after cecal ligation and puncture were substantially lower in C5aR- or C5L2-deficient mice as compared with that in C57BL/6J WT mice. These findings elucidate the functional characteristics of the C5L2 receptor during the acute inflammatory response.

Indexed as

Acute DiseaseAnimalsComplement C5aDisease Models, AnimalEnzyme-Linked Immunosorbent AssayGranulocyte Colony-Stimulating FactorInflammationMacrophages, PeritonealMiceMice, Inbred C57BLMice, KnockoutReal-Time Polymerase Chain ReactionReceptor, Anaphylatoxin C5aReceptors, ChemokineReceptors, ComplementSepsisC5AR1 protein, humanC5aR2 protein, humanComplement C5aGranulocyte Colony-Stimulating FactorReceptor, Anaphylatoxin C5aReceptors, ChemokineReceptors, ComplementAktCecal ligation and punctureMacrophagesMEK1/2Sepsis

Identifiers

PMID23575697
PMCPMC3795516
OpenAlexW1601934946

What OpenQuestion holds

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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.