Evidence map›Paper›PMID 21715328›Full record

ArticleThe Journal of biological chemistry2011

Leukotrienes target F-actin/cofilin-1 to enhance alveolar macrophage anti-fungal activity.

Mariana Morato-Marques, Marina R Campos, Steve Kane, Ana P Rangel, Casey Lewis, Megan N Ballinger, Sang-Hoon Kim, Marc Peters-Golden, Sonia Jancar, Carlos H Serezani

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.9field-weighted citation impact, top 10% 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, 40 citations in OpenAlex.

  1. Activation of leukotriene BCellular & molecular immunology · 2024
    Article
  2. Leukotrienes in Innate Immunity: Still Underappreciated after All These Years?Journal of immunology (Baltimore, Md. : 1950) · 2023
    Review
  3. Article
  4. Review
  5. Leukotriene BNature microbiology · 2019
    Article
  6. Article
  7. Article
  8. Article
  9. Too much of a good thing: How modulating LTBSeminars in immunology · 2017
    Review
  10. Macrophage LTBJournal of lipid research · 2017
    Article
  11. Host-Derived Leukotriene BFrontiers in immunology · 2017
    Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  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

10 authors at 2 institutions in 2 countries.

Mariana Morato-MarquesDepartment of Immunology, Institute of Biomedical Science IV, University of São Paulo, São Paulo 05508-900, Brazil.
Marina R CamposDepartment of Immunology, Institute of Biomedical Science IV, University of São Paulo, São Paulo 05508-900, Brazil.
Steve KaneDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Medical School, University of Michigan, Ann Arbor, Michigan 48109, and.
Ana P RangelDepartment of Immunology, Institute of Biomedical Science IV, University of São Paulo, São Paulo 05508-900, Brazil.
Casey LewisDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Medical School, University of Michigan, Ann Arbor, Michigan 48109, and.
Megan N BallingerDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Medical School, University of Michigan, Ann Arbor, Michigan 48109, and.
Sang-Hoon KimDivision of Allergy and Respiratory Medicine, Department of Internal Medicine, Eulji University School of Medicine, Seoul, 139-711, Republic of Korea.
Marc Peters-GoldenDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Medical School, University of Michigan, Ann Arbor, Michigan 48109, and.
Sonia JancarDepartment of Immunology, Institute of Biomedical Science IV, University of São Paulo, São Paulo 05508-900, Brazil.
Carlos H SerezaniDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Medical School, University of Michigan, Ann Arbor, Michigan 48109, and. Electronic address: cserezan@med.umich.edu.
University of Michigan–Ann Arbor · USEulji University · KR

Funding

LEUKOTRIENES AND PULMONARY ANTIBACTERIAL DEFENSER01HL058897 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PETERS-GOLDEN, MARC L · 1997 to 2012
$4.1M
Regulation of Toll-like receptor-induced NFkB activation by Gai-coupled receptorsR00HL103777 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI SEREZANI, C. HENRIQUE · 2012 to 2014
$713k
Eicosanoids and lung macrophage antimicrobial mechanismsR56HL058897 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PETERS-GOLDEN, MARC L · 2008 to 2008
$383k
Regulation of Toll-like receptor-induced NFkB activation by Gai-coupled receptorsK99HL103777 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SEREZANI, C. HENRIQUE · 2010 to 2011
$242k
NHLBI NIH HHS HL-058897NHLBI NIH HHS HL-103777-01NHLBI NIH HHS K99 HL103777NHLBI NIH HHS R00 HL103777NHLBI NIH HHS R01 HL058897NHLBI NIH HHS R56 HL058897
6 · The paper itself

Abstract

Candida albicans is the most common opportunistic fungal pathogen and causes local and systemic disease in immunocompromised patients. Alveolar macrophages (AMs) are pivotal for the clearance of C. albicans from the lung. Activated AMs secrete 5-lipoxygenase-derived leukotrienes (LTs), which in turn enhance phagocytosis and microbicidal activity against a diverse array of pathogens. Our aim was to investigate the role of LTB(4) and LTD(4) in AM antimicrobial functions against C. albicans and the signaling pathways involved. Pharmacologic and genetic inhibition of LT biosynthesis as well as receptor antagonism reduced phagocytosis of C. albicans when compared with untreated or WT controls. Conversely, exogenous LTs of both classes augmented base-line C. albicans phagocytosis by AMs. Although LTB(4) enhanced mainly mannose receptor-dependent fungal ingestion, LTD(4) enhanced mainly dectin-1 receptor-mediated phagocytosis. LT enhancement of yeast ingestion was dependent on protein kinase C-δ (PKCδ) and PI3K but not PKCα and MAPK activation. Both LTs reduced activation of cofilin-1, whereas they enhanced total cellular F-actin; however, LTB(4) accomplished this through the activation of LIM kinases (LIMKs) 1 and 2, whereas LTD(4) did so exclusively via LIMK-2. Finally, both exogenous LTB(4) and LTD(4) enhanced AM fungicidal activity in an NADPH oxidase-dependent manner. Our data identify LTB(4) and LTD(4) as key mediators of innate immunity against C. albicans, which act by both distinct and conserved signaling mechanisms to enhance multiple antimicrobial functions of AMs.

Indexed as

ActinsAnimalsCandida albicansCandidiasisCofilin 1Dectin-1Enzyme ActivationExtracellular Signal-Regulated MAP KinasesFemaleImmunity, InnateLectins, C-TypeLeukotriene B4Lim KinasesMacrophages, AlveolarMembrane ProteinsMiceActinsCfl1 protein, mouseCfl1 protein, ratCofilin 1Dectin-1Extracellular Signal-Regulated MAP KinasesLectins, C-TypeLeukotriene B4Lim KinasesMembrane ProteinsNerve Tissue ProteinsPhosphatidylinositol 3-KinasesProtein Kinase C-delta

Identifiers

PMID21715328
PMCPMC3190697
OpenAlexW2007900857

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.