Evidence map›Paper›PMID 26685897›Full record

ArticleLung2016

Decreased Bronchial Eosinophilic Inflammation and Mucus Hypersecretion in Asthmatic Mice Lacking All Nitric Oxide Synthase Isoforms.

Kentaro Akata, Kazuhiro Yatera, Ke-Yong Wang, Keisuke Naito, Takaaki Ogoshi, Shingo Noguchi, Takashi Kido, Yumiko Toyohira, Hiroaki Shimokawa, Nobuyuki Yanagihara and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Lung, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

10 citing papers in PubMed, 16 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

12 authors at 3 institutions in 1 country.

Kentaro AkataDepartment of Respiratory Medicine, University of Occupational and Environmental Health, Japan (UOEH), 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu, Fukuoka, 807-8555, Japan.
Kazuhiro YateraDepartment of Respiratory Medicine, University of Occupational and Environmental Health, Japan (UOEH), 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu, Fukuoka, 807-8555, Japan. yatera@med.uoeh-u.ac.jp.
Ke-Yong WangShared-Use Research Center, UOEH, Kitakyushu, Japan.
Keisuke NaitoDepartment of Respiratory Medicine, University of Occupational and Environmental Health, Japan (UOEH), 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu, Fukuoka, 807-8555, Japan.
Takaaki OgoshiDepartment of Respiratory Medicine, University of Occupational and Environmental Health, Japan (UOEH), 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu, Fukuoka, 807-8555, Japan.
Shingo NoguchiDepartment of Respiratory Medicine, University of Occupational and Environmental Health, Japan (UOEH), 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu, Fukuoka, 807-8555, Japan.
Takashi KidoDepartment of Respiratory Medicine, University of Occupational and Environmental Health, Japan (UOEH), 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu, Fukuoka, 807-8555, Japan.
Yumiko ToyohiraDepartment of Pharmacology, School of Medicine, UOEH, Kitakyushu, Japan.
Hiroaki ShimokawaDepartment of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
Nobuyuki YanagiharaDepartment of Pharmacology, School of Medicine, UOEH, Kitakyushu, Japan.
Masato TsutsuiDepartment of Pharmacology, Graduate School of Medicine, University of the Ryukyus, Okinawa, Japan.
Hiroshi MukaeDepartment of Respiratory Medicine, University of Occupational and Environmental Health, Japan (UOEH), 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu, Fukuoka, 807-8555, Japan.
University of Occupational and Environmental Health Japan · JPTohoku University · JPUniversity of the Ryukyus · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAsthma is characterized by airflow limitation with chronic airway inflammation, hyperresponsiveness and mucus hypersecretion. NO is generated by three nitric oxide synthase (i/n/eNOSs) isoforms, but conflicting results have been reported using asthmatic mice treated with NOSs inhibitors and NOS-knockout mice. To elucidate the authentic role of NO/NOSs in asthma, we used asthmatic mice lacking all NOSs (n/i/eNOS(-/-)).

methodsWild-type and n/i/eNOS(-/-) mice were sensitized and challenged with ovalbumin. Pathological findings and expressions of interferon (IFN)-γ, interleukin (IL)-4, -5, -10, -13 and chemokines in the lung were evaluated.

resultsDecreased eosinophilic inflammation, bronchial thickening and mucus secretion, IL-4, -5 and -13, monocyte chemoattractant protein-1, eotaxin-1 and thymus and activation-regulated chemokine expressions were observed in n/i/eNOS(-/-) mice compared to wild-type, but expressions of IFN-γ and IL-10 were similar.

conclusionUsing asthmatic n/i/eNOS(-/-) mice, NO plays important roles in accelerating bronchial eosinophilic inflammation and mucus hypersecretion in the pathophysiology of asthma.

Indexed as

AnimalsAsthmaBronchitisChemokine CCL11Chemokine CCL17Chemokine CCL2CytokinesEosinophilsGene ExpressionInterferon-gammaInterleukin-10Interleukin-13Interleukin-4Interleukin-5MaleMiceCcl17 protein, mouseChemokine CCL11Chemokine CCL17Chemokine CCL2CytokinesInterferon-gammaInterleukin-10Interleukin-13Interleukin-4Interleukin-5Nitric Oxide SynthaseRNA, MessengerBronchial asthmaEosinophilic inflammationNitric oxideNitric oxide synthase

Identifiers

PMID26685897
OpenAlexW2206976517

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.