Evidence map›Paper›PMID 9784515›Full record

ArticleInfection and immunity1998

5-Lipoxygenase reaction products modulate alveolar macrophage phagocytosis of Klebsiella pneumoniae.

P Mancuso, T J Standiford, T Marshall, M Peters-Golden

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.

  1. Metabolites of prostaglandin synthases as potential biomarkers of Lyme disease severity and symptom resolution.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Pooled it
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  8. Leptin MediatesFrontiers in immunology · 2018
    Article
  9. Too much of a good thing: How modulating LTBSeminars in immunology · 2017
    Review
  10. Macrophage LTBJournal of lipid research · 2017
    Article
  11. Article
  12. Article
  13. Article
  14. Dynamics of Increasing IFN-γ Exposure on Murine MH-S Cell-Line Alveolar Macrophage Phagocytosis of Streptococcus pneumoniae.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2015
    Article
  15. Article
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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

4 authors at 1 institution in 1 country.

P MancusoDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Michigan 48109-0642, USA. petersm@medmail.med.umich.edu
T J Standiford
T Marshall
M Peters-Golden
University of Michigan–Ann Arbor · US

Funding

PULMONARY CELLULAR AND MOLECULAR BIOLOGY TRAININGT32HL007749 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Robert Pickett Dickson · 1993 to 2026
$19.9M
LEUKOTRIENES AND PULMONARY ANTIBACTERIAL DEFENSER01HL058897 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PETERS-GOLDEN, MARC L · 1997 to 2012
$4.1M
NHLBI NIH HHS R01 HL058897NHLBI NIH HHS R01-HL58897NHLBI NIH HHS T32 HL007749NHLBI NIH HHS T32 HL07749
6 · The paper itself

Abstract

The leukotrienes are potent lipid mediators of inflammation formed by the 5-lipoxygenase-catalyzed oxidation of arachidonic acid. Although the effects of leukotrienes on neutrophil chemotaxis and activation have been established, their role in modulating innate host defense mechanisms is poorly understood. In a previous study (M. Bailie, T. Standiford, L. Laichalk, M. Coffey, R. Strieter, and M. Peters-Golden, J. Immunol. 157:5221-5224, 1996), we used 5-lipoxygenase knockout mice to establish a critical role for endogenous leukotrienes in pulmonary clearance and alveolar macrophage phagocytosis of Klebsiella pneumoniae. In the present study, we investigated the role of specific endogenous leukotrienes in phagocytosis of K. pneumoniae and explored the possibility that exogenous leukotrienes could restore phagocytosis in alveolar macrophages with endogenous leukotriene synthesis inhibition and enhance this process in leukotriene-competent cells. Rat alveolar macrophages produced leukotriene B4 (LTB4), LTC4, and 5-hydoxyeicosatetraenoic acid (5-HETE) during the process of phagocytosis, and the inhibition of endogenous leukotriene synthesis with zileuton and MK-886 dramatically attenuated phagocytosis. We also observed a reduction in phagocytosis when we treated alveolar macrophages with antagonists to the plasma membrane receptors for either LTB4, cysteinyl-leukotrienes, or both. In leukotriene-competent cells, LTC4 augmented phagocytosis to the greatest extent, followed by 5-HETE and LTB4. These 5-lipoxygenase reaction products demonstrated similar relative abilities to reconstitute phagocytosis in zileuton-treated rat alveolar macrophages and in alveolar macrophages from 5-lipoxygenase knockout mice. We conclude that endogenous synthesis of all major 5-lipoxygenase reaction products plays an essential role in phagocytosis. The restorative and pharmacologic effects of LTC4, LTB4, and 5-HETE may provide a basis for their exogenous administration as an adjunctive treatment for patients with gram-negative bacterial pneumonia.

Indexed as

AnimalsArachidonate 5-LipoxygenaseFemaleKlebsiella pneumoniaeLeukotriene AntagonistsLeukotrienesMacrophages, AlveolarMiceMice, KnockoutOpsonin ProteinsPhagocytosisRatsRats, WistarReceptors, Cell SurfaceArachidonate 5-LipoxygenaseLeukotriene AntagonistsLeukotrienesOpsonin ProteinsReceptors, Cell Surface

Identifiers

PMID9784515
PMCPMC108641
OpenAlexW2151702529

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.