Evidence map›Paper›PMID 25689617›Full record

ArticleCytokine2015

Orosomucoid 1 drives opportunistic infections through the polarization of monocytes to the M2b phenotype.

Kiwamu Nakamura, Ichiaki Ito, Makiko Kobayashi, David N Herndon, Fujio Suzuki

Open access · greenAbstract read
In one paragraph

Article in Cytokine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. CD34Cells · 2022
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. αKidney360 · 2020
    Article
  16. Article
  17. Article
  18. M2b macrophage polarization and its roles in diseases.Journal of leukocyte biology · 2019
    Review
  19. Article
  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

5 authors at 2 institutions in 1 country.

Kiwamu NakamuraDepartment of Internal Medicine, The University of Texas Medical Branch, Galveston, TX 77555, United States.
Ichiaki ItoDepartment of Internal Medicine, The University of Texas Medical Branch, Galveston, TX 77555, United States.
Makiko KobayashiDepartment of Internal Medicine, The University of Texas Medical Branch, Galveston, TX 77555, United States; Shriners Hospital for Children, Galveston, TX 77550, United States.
David N HerndonShriners Hospital for Children, Galveston, TX 77550, United States.
Fujio SuzukiDepartment of Internal Medicine, The University of Texas Medical Branch, Galveston, TX 77555, United States; Shriners Hospital for Children, Galveston, TX 77550, United States. Electronic address: fsuzuki@utmb.edu.
The University of Texas Medical Branch at Galveston · USShriners Hospitals for Children - Galveston · US

Funding

Project 9: The role of androgen/corticosteroid in fat, muscle and glucose metabolism of burn victimsP50GM060338 · NIGMS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI SZABO, CSABA · 2000 to 2017
$24.2M
NIGMS NIH HHS P50 GM060338
6 · The paper itself

Abstract

Orosomucoid (ORM, composed of two isoforms, ORM1 and ORM2) has been described as an inducer of M2 macrophages, which are cells that decrease host antibacterial innate immunities. However, it is unknown which phenotypes of M2 macrophages are induced by ORM. In this study, healthy donor monocytes stimulated with ORM (ORM-monocytes) were characterized phenotypically and biologically. CCL1 (a biomarker of M2b macrophages) and IL-10 were detected in monocyte cultures supplemented with ORM1; however, CCL17 (a biomarker of M2a macrophages) and CXCL13 (a biomarker of M2c macrophages) were not produced in these cultures. All of these soluble factors were not detected in the culture fluids of monocytes stimulated with ORM2. Monocytes stimulated with ORM1 were characterized as CD64(-)CD209(-)CD163(+)CCL1(+) cells. MRSA and Enterococcus faecalis infections were accelerated in chimeras (NOD/scid IL-2Rγ(null) mice reconstituted with white blood cells) after inoculation with monocytes stimulated with ORM1 or treatment with ORM1; however, the infections were greatly mitigated in both chimeras inoculated with ORM1-stimulated monocytes and treated with ORM1, after an additional treatment with an inhibitor of M2b macrophages (CCL1 antisense ODN). These results indicate that ORM1 stimulates quiescent monocytes to polarize to M2b monocytes. The regulation of M2b macrophages may be beneficial in controlling opportunistic infections in patients with a large amount of plasma ORM1.

Indexed as

AnimalsCell PolarityCells, CulturedChemokinesEnterococcus faecalisHumansMethicillin-Resistant Staphylococcus aureusMiceMonocytesOpportunistic InfectionsOrosomucoidPhenotypeChemokinesOrosomucoidCCL1MonocytesOrosomucoid

Identifiers

PMID25689617
PMCPMC4541791
OpenAlexW2072769614

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.