Evidence map›Paper›PMID 21859896›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011

MyD88-dependent production of IL-17F is modulated by the anaphylatoxin C5a via the Akt signaling pathway.

Markus Bosmann, Vinay R Patel, Norman F Russkamp, Florence Pache, Firas S Zetoune, J Vidya Sarma, Peter A Ward

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. 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
1.9field-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, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. 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
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Complement-induced activation of MAPKs and Akt during sepsis: role in cardiac dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Potential role of myeloid cell/eosinophil-derived IL-17 in LPS-induced endotoxin shock.Biochemical and biophysical research communications · 2014
    Article
  16. Article
  17. Article
  18. New developments in C5a receptor signaling.Cell health and cytoskeleton · 2012
    Article
  19. Article
  20. Anti-inflammatory effects of β2 adrenergic receptor agonists in experimental acute lung injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012
    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

7 authors at 1 institution in 1 country.

Markus BosmannDepartment of Pathology, The University of Michigan Medical School, 1301 Catherine Rd., Ann Arbor, MI 48109-5602, USA.
Vinay R Patel
Norman F Russkamp
Florence Pache
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 interleukin-17 (IL-17) family of cytokines plays important roles in innate immune defenses against bacterial and fungal pathogens. While much is known about IL-17A, much less information is available about the IL-17F isoform. Here, we investigated gene expression and release of IL-17F and its regulation by the complement system. IL-17F was produced in mouse peritoneal elicited macrophages after TLR4 activation by LPS, peaking after 12 h. This effect was completely dependent on the presence of the adaptor protein MyD88. The copresence of the complement activation product, C5a (EC(50)=10 nM), amplified IL-17F production via the receptor C5aR. In vitro signaling studies indicated that LPS or C5a, or the combination, caused phosphorylation of Akt occurring at threonine 308 but not at serine 473. Treatment of macrophages with pharmacologic inhibitors of PI3K-Akt greatly reduced production of IL-17F as well as mRNA for IL-17F. In endotoxemia, C5a levels peaked at 6 h, while IL-17F levels peaked between 6-12 h. Full in vivo production of IL-17F during endotoxemia required C5a. A similar result was found in the cecal ligation and puncture sepsis model. These data suggest that maximal production of IL-17F requires complement activation and presence of C5a.

Indexed as

AnimalsComplement ActivationComplement C5aEndotoxemiaImmunity, InnateInterleukin-17Macrophages, PeritonealMaleMiceMice, Inbred C57BLMice, KnockoutMyeloid Differentiation Factor 88Proto-Oncogene Proteins c-aktRNA, MessengerSignal TransductionToll-Like Receptor 4Complement C5aIl17f protein, mouseInterleukin-17Myd88 protein, mouseMyeloid Differentiation Factor 88Proto-Oncogene Proteins c-aktRNA, MessengerTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID21859896
PMCPMC3236631
OpenAlexW2081448804

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.