Evidence map›Paper›PMID 12414531›Full record

ArticleThe American journal of pathology2002

Generation of C5a by phagocytic cells.

Markus Huber-Lang, Ellen M Younkin, J Vidya Sarma, Niels Riedemann, Stephanie R McGuire, Kristina T Lu, Robin Kunkel, John G Younger, Firas S Zetoune, Peter A Ward

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

96 citing papers in PubMed, 209 citations in OpenAlex.

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  17. Skin-homing basophils and beyond.Frontiers in immunology · 2022
    Article
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  19. Article
  20. Article

36 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

10 authors at 1 institution in 1 country.

Markus Huber-LangDepartment of Pathology, University of Michigan Medical School, Ann Arbor 48109, USA.
Ellen M Younkin
J Vidya Sarma
Niels Riedemann
Stephanie R McGuire
Kristina T Lu
Robin Kunkel
John G Younger
Firas S Zetoune
Peter A Ward
University of Michigan–Ann Arbor · US

Funding

MONONUCLEAR LEUKOCYTE ADHESION AND RECRUITMENT IN CHRONIC INFLAMMATORY DISEASEP01HL031963 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JOHNSON, KENT JOHN · 1985 to 2009
$14.1M
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
LUNG INJURY BY OXYGEN METABOLITESR37GM029507 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WARD, PETER A · 1987 to 1996
–
NHLBI NIH HHS HL-31963NHLBI NIH HHS P01 HL031963NIGMS NIH HHS GM-29507NIGMS NIH HHS R01 GM029507NIGMS NIH HHS R37 GM029507
6 · The paper itself

Abstract

The complement activation product, C5a, is a powerful phlogistic factor. Using antibodies to detect human or rat C5a, incubation at pH 7.4 of human blood neutrophils or rat alveolar macrophages (AMs) with C5 in the presence of phorbol 12-myristate 13-acetate (PMA) led to generation of C5a. Rat AMs activated with lipopolysaccharide also generated C5a from C5. With activated neutrophils, extensive cleavage of C5 occurred, whereas activated macrophages had much more selective proteolytic activity for C5. Peripheral blood human or rat mononuclear cells and rat alveolar epithelial cells when stimulated with phorbol ester all failed to demonstrate an ability to cleave C5, suggesting a specificity of C5 cleavage by phagocytic cells. With rat AMs, C5a generation was time-dependent and was blocked if AMs were pretreated with inhibitors of transcription or protein synthesis (actinomycin D or cycloheximide). Similar treatment of activated human polymorphonuclear leukocytes only partially reduced C5a generation after addition of C5. C5a generated by activated AMs was biologically (chemotactically) active. This generation was sensitive to serine protease inhibitors but not to other classes of inhibitors. These data indicate that phagocytic cells, especially lung macrophages, can generate C5a from C5. In the context of the lung, this may represent an important C5a-generating pathway that is independent of the plasma complement system.

Indexed as

AnimalsCells, CulturedChemotaxisComplement C5Complement C5aComplement Hemolytic Activity AssayEnzyme InhibitorsHumansKineticsLungMacrophages, AlveolarNeutrophilsPhagocytesProteinase Inhibitory Proteins, SecretoryProteinsProtein Synthesis InhibitorsComplement C5Complement C5aEnzyme InhibitorsProteinase Inhibitory Proteins, SecretoryProteinsProtein Synthesis InhibitorsSerine Proteinase InhibitorsTrypsin Inhibitors

Identifiers

PMID12414531
PMCPMC1850785
OpenAlexW2088926833

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.