Evidence map›Paper›PMID 8757859›Full record

ArticleInfection and immunity1996

Roles for tumor necrosis factor alpha and nitric oxide in resistance of rat alveolar macrophages to Legionella pneumophila.

S J Skerrett, T R Martin

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 63 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

S J SkerrettMedical Research Service, Veterans Affairs Medical Center, Seattle, Washington 98108, USA.
T R Martin
Veterans Health Administration · US

Funding

TOXIC OXYGEN PRODUCTS AND PULMONARY EDEMAP50HL030542 · NHLBI · UNIVERSITY OF WASHINGTON · PI HUDSON, LEONARD D · 1985 to 2003
$6.1M
ALVEOLAR MACROPHAGE-DERIVED NEUTROPHIL CHEMOATTRACTANTR01AI029103 · NIAID · UNIVERSITY OF WASHINGTON · PI MARTIN, THOMAS R · 1990 to 1998
–
NHLBI NIH HHS HL 30542NIAID NIH HHS AI 29103
6 · The paper itself

Abstract

Legionella pneumophila is an intracellular parasite of alveolar macrophages, and recovery from legionellosis is associated with activation of alveolar macrophages to resist intracellular bacterial replication. Gamma interferon (IFN-gamma) is known to activate alveolar macrophages to suppress L. pneumophila, but the role of macrophage-derived cytokines in modulating alveolar macrophage resistance is unknown. To test the hypothesis that macrophage-derived mediators contribute to the resistance of alveolar macrophages to L. pneumophila, we incubated adherent rat alveolar macrophages with Escherichia coli lipopolysaccharide (LPS), recombinant tumor necrosis factor alpha (TNF-alpha), recombinant IFN-gamma, neutralizing anti-TNF-alpha, and/or N(G)-monomethyl-L-arginine (L-NMMA) for 6 h before challenge with L. pneumophila. Monolayers were sonically disrupted and quantitatively cultured on successive days. We also measured bioactive TNF-alpha release by infected macrophages in the presence or absence of IFN-gamma. We found that pretreatment of alveolar macrophages with LPS or, to a lesser degree, TNF-alpha, significantly inhibited intracellular replication of L. pneumophila. Both LPS and TNF-alpha acted synergistically with IFN-gamma at less than the maximally activating concentration to suppress L. pneumophila growth. The independent and coactivating effects of LPS were blocked by anti-TNF-alpha. Killing of L. pneumophila by IFN-gamma at the maximally activating concentration was inhibited by anti-TNF-alpha. The synergistic effects of TNF-alpha. or LPS in combination with IFN-gamma were inhibited by L-NMMA. Infected alveolar macrophages secreted TNF-alpha in proportion to the bacterial inoculum, and secretion of TNF-alpha was potentiated by cocultivation with IFN-gamma. These data indicate that secretion of TNF-alpha is an important autocrine defense mechanism of alveolar macrophages, serving to potentiate the activating effects of IFN-gamma through costimulation of nitric oxide synthesis.

Indexed as

AnimalsArginineColony Count, MicrobialEndotoxinsImmunity, InnateInterferon-gammaLegionella pneumophilaLegionnaires' DiseaseLipopolysaccharidesMacrophage ActivationMacrophages, AlveolarMaleNitric Oxideomega-N-MethylarginineRatsRats, Sprague-DawleyArginineEndotoxinsInterferon-gammaLipopolysaccharidesNitric Oxideomega-N-MethylarginineTumor Necrosis Factor-alpha

Identifiers

PMID8757859
PMCPMC174213
OpenAlexW2163374608

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.