Evidence map›Paper›PMID 31302837›Full record

ArticleSleep & breathing = Schlaf & Atmung2020

Exposure to intermittent hypoxia inhibits allergic airway inflammation in a murine model of asthma.

Shin Ohta, Akihiko Tanaka, Megumi Jinno, Kuniaki Hirai, Yoshito Miyata, Munehiro Yamaguchi, Tetsuya Homma, Mayumi Muramoto, Yoshio Watanabe, Shintaro Suzuki and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Sleep & breathing = Schlaf & Atmung, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 40% 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, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
  2. Review
  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

12 authors at 1 institution in 1 country.

Shin OhtaDepartment of Internal Medicine, Division of Respiratory Medicine and Allergology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8666, Japan. shinohta@med.showa-u.ac.jp.ORCID http://orcid.org/0000-0001-8744-6096
Akihiko TanakaDepartment of Internal Medicine, Division of Respiratory Medicine and Allergology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8666, Japan.
Megumi JinnoDepartment of Internal Medicine, Division of Respiratory Medicine and Allergology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8666, Japan.
Kuniaki HiraiDepartment of Internal Medicine, Division of Respiratory Medicine and Allergology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8666, Japan.
Yoshito MiyataDepartment of Internal Medicine, Division of Respiratory Medicine and Allergology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8666, Japan.
Munehiro YamaguchiDepartment of Internal Medicine, Division of Respiratory Medicine and Allergology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8666, Japan.
Tetsuya HommaDepartment of Internal Medicine, Division of Respiratory Medicine and Allergology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8666, Japan.
Mayumi MuramotoDepartment of Internal Medicine, Division of Respiratory Medicine and Allergology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8666, Japan.
Yoshio WatanabeDepartment of Internal Medicine, Division of Respiratory Medicine and Allergology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8666, Japan.
Shintaro SuzukiDepartment of Internal Medicine, Division of Respiratory Medicine and Allergology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8666, Japan.
Takuya YokoeDepartment of Internal Medicine, Division of Respiratory Medicine and Allergology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8666, Japan.
Hironori SagaraDepartment of Internal Medicine, Division of Respiratory Medicine and Allergology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8666, Japan.
Showa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeObesity increases the severity of asthma, and patients with severe asthma are often complicated with obstructive sleep apnea syndrome (OSAS), a concomitant disease of obesity. We investigated whether intermittent hypoxia (IH), which is a physiological feature of OSAS, modifies allergic airway inflammation in a murine model of asthma.

methodsBalb/c mice were sensitized by ovalbumin (OVA) intraperitoneally twice (days 1 and 14) and challenged with intranasal OVA three times (days 21, 22, and 23). The mice were exposed to IH either from days 1 to 24 (long exposure) or only from days 21 to 24 (short exposure). The impact of IH exposure to allergic airway inflammation was investigated using these mice models by histologic, morphometric, and molecular techniques. Additionally, the airway responsiveness to acetylcholine was also assessed.

resultsOVA-sensitized and OVA-challenged mice exposed to room air (RA) showed increased total cell and eosinophil numbers in the BALF. The levels of interleukin (IL)-5 and IL-13 in the BALF also increased and goblet cell metaplasia was induced. In contrast, both long and short exposure to IH inhibited the increased total cell and eosinophil numbers. The levels of IL-5 and IL-13 in the BALF also decreased on exposure to IH. Moreover, the goblet cell hyperplasia and airway hyperresponsiveness were significantly reduced in mice exposed to IH compared to those exposed to RA.

conclusionsThese results suggest that IH may not deteriorate the asthmatic condition in a murine model of asthma.

Indexed as

AnimalsAsthmaDisease Models, AnimalFemaleHypoxiaInflammationMiceMice, Inbred BALB CRespiratory HypersensitivitySleep Apnea, ObstructiveAllergic airway inflammationAnimal modelAsthmaIntermittent hypoxiaSleep apnea syndrome

Identifiers

PMID31302837
OpenAlexW2958322329

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.