Evidence map›Paper›PMID 30365491›Full record

ArticlePloS one2018

NLRP3/Caspase-1 inflammasome activation is decreased in alveolar macrophages in patients with lung cancer.

Ismini Lasithiotaki, Eliza Tsitoura, Katerina D Samara, Athina Trachalaki, Irini Charalambous, Nikolaos Tzanakis, Katerina M Antoniou

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2018. 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
1.3field-weighted citation impact, top 19% 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, 57 citations in OpenAlex.

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  8. Review
  9. Divergent functions of NLRP3 inflammasomes in cancer: a review.Cell communication and signaling : CCS · 2023
    Review
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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

7 authors at 1 institution in 1 country.

Ismini LasithiotakiLaboratory of Cellular and Molecular Pulmonology, Medical School, University of Crete, Heraklion, Crete, Greece.ORCID 0000-0001-5089-7547
Eliza TsitouraLaboratory of Cellular and Molecular Pulmonology, Medical School, University of Crete, Heraklion, Crete, Greece.
Katerina D SamaraLaboratory of Cellular and Molecular Pulmonology, Medical School, University of Crete, Heraklion, Crete, Greece.
Athina TrachalakiLaboratory of Cellular and Molecular Pulmonology, Medical School, University of Crete, Heraklion, Crete, Greece.
Irini CharalambousLaboratory of Cellular and Molecular Pulmonology, Medical School, University of Crete, Heraklion, Crete, Greece.
Nikolaos TzanakisLaboratory of Cellular and Molecular Pulmonology, Medical School, University of Crete, Heraklion, Crete, Greece.
Katerina M AntoniouLaboratory of Cellular and Molecular Pulmonology, Medical School, University of Crete, Heraklion, Crete, Greece.
University of Crete · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer (LC) remains the leading cause of cancer-related mortality. The interaction of cancer cells with their microenvironment, results in tumor escape or elimination. Alveolar macrophages (AMs) play a significant role in lung immunoregulation, however their role in LC has been outshined by the study of tumor associated macrophages. Inflammasomes are key components of innate immune responses and can exert either tumor-suppressive or oncogenic functions, while their role in lung cancer is largely unknown. We thus investigated the NLRP3 pathway in Bronchoalveolar Lavage derived alveolar macrophages and peripheral blood leukocytes from patients with primary lung cancer and healthy individuals. IL-1β and IL-18 secretion was significantly higher in unstimulated peripheral blood leukocytes from LC patients, while IL-1β secretion could be further increased upon NLRP3 stimulation. In contrast, in LC AMs, we observed a different profile of IL-1β secretion, characterized mainly by the impairment of IL-1β production in NLRP3 stimulated cells. AMs also exhibited an impaired TLR4/LPS pathway as shown by the reduced induction of IL-6 and TNF-α. Our results support the hypothesis of tumour induced immunosuppression in the lung microenvironment and may provide novel targets for cancer immunotherapy.

Indexed as

AgedBronchoalveolar Lavage FluidCarcinoma, Non-Small-Cell LungCase-Control StudiesCaspase 1FemaleHealthy VolunteersHumansImmune ToleranceInflammasomesInterleukin-18Interleukin-1betaLungLung NeoplasmsMacrophages, AlveolarMaleCaspase 1IL1B protein, humanInflammasomesInterleukin-18Interleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, human

Identifiers

PMID30365491
PMCPMC6203254
OpenAlexW2898306085

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.