Evidence map›Paper›PMID 26067998›Full record

ArticlePloS one2015

Invariant Natural Killer T Cells Play a Role in Chemotaxis, Complement Activation and Mucus Production in a Mouse Model of Airway Hyperreactivity and Inflammation.

Piia Karisola, Maili Lehto, Pia Kinaret, Niina Ahonen, Rita Haapakoski, Minna Anthoni, Masaru Taniguchi, Henrik Wolff, Anne Puustinen, Harri Alenius

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Article
  3. 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.

Piia KarisolaUnit of Systems Toxicology, Finnish Institute of Occupational Health, Helsinki, Finland.
Maili LehtoUnit of Systems Toxicology, Finnish Institute of Occupational Health, Helsinki, Finland.
Pia KinaretUnit of Systems Toxicology, Finnish Institute of Occupational Health, Helsinki, Finland.
Niina AhonenUnit of Systems Toxicology, Finnish Institute of Occupational Health, Helsinki, Finland.
Rita HaapakoskiUnit of Systems Toxicology, Finnish Institute of Occupational Health, Helsinki, Finland.
Minna AnthoniUnit of Systems Toxicology, Finnish Institute of Occupational Health, Helsinki, Finland.
Masaru TaniguchiRIKEN Center for Integrative Medical Sciences, Laboratory for Immune Regulation, RCAI Kanagawa, Japan.
Henrik WolffUnit of Systems Toxicology, Finnish Institute of Occupational Health, Helsinki, Finland.
Anne PuustinenUnit of Systems Toxicology, Finnish Institute of Occupational Health, Helsinki, Finland.
Harri AleniusUnit of Systems Toxicology, Finnish Institute of Occupational Health, Helsinki, Finland.
Finnish Institute of Occupational Health · FIRIKEN Center for Integrative Medical Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD1d-restricted invariant natural killer T (iNKT) cells play a critical role in the induction of airway hyperreactivity (AHR). After intranasal alpha-galactosylceramide (α-GalCer) administration, bronchoalveolar lavage fluid (BALF) proteins from mouse lung were resolved by two-dimensional differential gel electrophoresis (2D-DIGE), and identified by tandem mass spectroscopy. A lack of iNKT cells prevented the development of airway responses including AHR, neutrophilia and the production of the proinflammatory cytokines in lungs. Differentially abundant proteins in the BALF proteome of α-GalCer-treated wild type mice included lungkine (CXCL15), pulmonary surfactant-associated protein D (SFTPD), calcium-activated chloride channel regulator 1 (CLCA1), fragments of complement 3, chitinase 3-like proteins 1 (CH3LI) and 3 (CH3L3) and neutrophil gelatinase-associated lipocalin (NGAL). These proteins may contribute to iNKT regulated AHR via several mechanisms: altering leukocyte chemotaxis, increasing airway mucus production and possibly via complement activation.

Indexed as

ChemotaxisComplement ActivationAcute-Phase ProteinsAnimalsbeta-N-AcetylhexosaminidasesChemokines, CXCChitinase-3-Like Protein 1Complement C3FemaleGlycoproteinsInflammationKiller Cells, NaturalLectinsLipocalin-2LipocalinsMiceAcute-Phase Proteinsbeta-N-AcetylhexosaminidasesChemokines, CXCChil1 protein, mouseChil3 protein, mouseChitinase-3-Like Protein 1Complement C3Cxcl15 protein, mouseGlycoproteinsLcn2 protein, mouseLectinsLipocalin-2LipocalinsOncogene ProteinsPulmonary Surfactant-Associated Protein D

Identifiers

PMID26067998
PMCPMC4466557
OpenAlexW608192047

What OpenQuestion holds

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LicenceCC BY
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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.