Evidence map›Paper›PMID 20959460›Full record

ArticleThe Journal of biological chemistry2010

Leukotriene B4 augments and restores Fc gammaRs-dependent phagocytosis in macrophages.

Fuyuki Okamoto, Kazuko Saeki, Hideki Sumimoto, Sho Yamasaki, Takehiko Yokomizo

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. Activation of leukotriene BCellular & molecular immunology · 2024
    Article
  3. Article
  4. Candida albicans-induced leukotriene biosynthesis in neutrophils is restricted to the hyphal morphology.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  5. Expression of leukotriene BCellular & molecular immunology · 2021
    Article
  6. Article
  7. Article
  8. Article
  9. Leukotriene receptors as potential therapeutic targets.The Journal of clinical investigation · 2018
    Review
  10. Article
  11. Article
  12. Macrophage LTBJournal of lipid research · 2017
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  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.

Fuyuki OkamotoDepartment of Medical Biochemistry, Graduate School of Medical Sciences, Kyushu University, Higashi-ku, Fukuoka 812-8582, Japan.
Kazuko Saeki
Hideki Sumimoto
Sho Yamasaki
Takehiko Yokomizo
Kyushu University · JPJapan Science and Technology Agency · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phagocytosis by macrophages is essential for host defense, i.e. preventing invasion of pathogens and foreign materials. Macrophages engulf immunoglobulin G (IgG)-opsonized particles through the action of the receptors for the Fc of IgG (FcγRs). Leukotriene B(4) (LTB(4)) is a classical lipid chemoattractant derived from arachidonic acid. Leukotriene B(4) receptor 1 (BLT1), a high affinity LTB(4) receptor, is expressed in a variety of immune cells such as neutrophils, macrophages, and dendritic cells. Although LTB(4) has been shown to enhance macrophage phagocytosis, few studies have investigated the intracellular mechanisms involved in this in detail. Furthermore, there have been no reports of the direct cross-talk between LTB(4)-BLT1 and IgG-FcγRs signaling. Here, we show that FcγRs-dependent phagocytosis was attenuated in BLT1-deficient macrophages as compared with wild-type (WT) cells. Moreover, cross-talk between LTB(4)-BLT1 and IgG-FcγRs signaling was identified at the level of phosphatidylinositol 3-OH kinase (PI3K) and Rac, downstream of Syk. In addition, the trimeric G(i) protein (G(i)) was found to be essential for BLT1-dependent phagocytosis. Surprisingly, we found that LTB(4)-BLT1 signaling restores phagocytosis in the absence of FcγRs signaling. These data indicate that LTB(4)-BLT1 signaling plays a pivotal role in macrophage phagocytosis and innate immunity.

Indexed as

AnimalsGene Expression RegulationGTP-Binding Protein alpha Subunits, Gi-GoImmunity, InnateIntracellular Signaling Peptides and ProteinsLeukotriene B4MacrophagesMiceMice, Mutant StrainsPhagocytosisPhosphatidylinositol 3-KinasesProtein-Tyrosine KinasesProto-Oncogene Proteins c-aktReceptors, IgGReceptors, Leukotriene B4Signal TransductionGTP-Binding Protein alpha Subunits, Gi-GoIntracellular Signaling Peptides and ProteinsLeukotriene B4Ltb4r1 protein, mousePhosphatidylinositol 3-KinasesProtein-Tyrosine KinasesProto-Oncogene Proteins c-aktReceptors, IgGReceptors, Leukotriene B4Syk KinaseSyk protein, mouse

Identifiers

PMID20959460
PMCPMC3003409
OpenAlexW2002569735

What Socratic 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 Socratic graph.