Evidence map›Paper›PMID 30764556›Full record

ArticleMedical sciences (Basel, Switzerland)2019

Eosinophilic Upper Airway Inflammation in a Murine Model Using an Adoptive Transfer System Induces Hyposmia and Epithelial Layer Injury with Convex Lesions.

Akira Kanda, Kenji Kondo, Naoki Hosaka, Yoshiki Kobayashi, Dan Van Bui, Yasutaka Yun, Kensuke Suzuki, Shunsuke Sawada, Mikiya Asako, Akihiko Nakamura and 7 more

Open access · goldAbstract read
In one paragraph

Article in Medical sciences (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

1 citing paper in PubMed, 8 citations in OpenAlex.

  1. 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

17 authors at 7 institutions in 2 countries.

Akira KandaDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Hirakata 573-1010, Japan. akanda@hirakata.kmu.ac.jp.ORCID 0000-0001-6324-721X
Kenji KondoDepartment of Otolaryngology and Head and Neck Surgery, Graduate School of Medicine, the University of Tokyo Hospital, Tokyo, 113-8655, Japan. kondok-tky@umin.ac.jp.
Naoki HosakaDepartment of Pathology, Fuchu Hospital, Izumi 594-0076, Japan. hosakan@hirakata.kmu.ac.jp.
Yoshiki KobayashiDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Hirakata 573-1010, Japan. kobayosh@hirakata.kmu.ac.jp.ORCID 0000-0003-3755-3074
Dan Van BuiDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Hirakata 573-1010, Japan. buivanda@hirakata.kmu.ac.jp.
Yasutaka YunDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Hirakata 573-1010, Japan. yunys@hirakata.kmu.ac.jp.
Kensuke SuzukiDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Hirakata 573-1010, Japan. suzukken@hirakata.kmu.ac.jp.ORCID 0000-0003-1659-1549
Shunsuke SawadaDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Hirakata 573-1010, Japan. sawadash@hirakata.kmu.ac.jp.
Mikiya AsakoDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Hirakata 573-1010, Japan. asako@hirakata.kmu.ac.jp.
Akihiko NakamuraNakamura ENT Clinic, Sakai 591-8025, Japan. nakamura-ent@paw.hi-ho.ne.jp.
Koichi TomodaDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Hirakata 573-1010, Japan. tomodak@hirakata.kmu.ac.jp.
Yoshiko SakataCentral Research Laboratory, Kansai Medical University, Hirakata 573-1010, Japan. sakatayo@hirakata.kmu.ac.jp.
Koji TsutaDepartment of Pathology, Kansai Medical University, Hirakata 573-1010, Japan. tsutakoj@hirakata.kmu.ac.jp.
David DombrowiczEGID, Inserm, CHU Lille, Institut Pasteur de Lille, U1011, University of Lille, 59019 Lille, France. david.dombrowicz@pasteur-lille.fr.
Hideyuki KawauchiDepartment of Otorhinolaryngology, Shimane University Faculty of Medicine, Izumo 693-0021, Japan. kawauchi@med.shimane-u.ac.jp.ORCID 0000-0003-4161-2591
Shigeharu FujiedaDepartment of Otorhinolaryngology Head & Neck Surgery, University of Fukui, Fukui 910-1193, Japan. sfujieda@g.u-fukui.ac.jp.
Hiroshi IwaiDepartment of Otolaryngology, Head and Neck Surgery, Kansai Medical University, Hirakata 573-1010, Japan. iwai@hirakata.kmu.ac.jp.
Kansai Medical University · JPFuchu Hospital · JPInserm · FRShimane University · JPThe Nakamura Hajime Eastern Institute · JPUniversity of Fukui · JPUniversity of Tokyo Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic rhinosinusitis with nasal polyps (CRSwNP) is a refractory upper airway disease, accompanied mainly by eosinophilia and/or asthma. In addition, the disease correlates with a high rate of hyposmia, following a marked infiltration of eosinophils into the inflamed site, the paranasal sinus. Although eosinophils are known to contribute to the development of hyposmia and CRSwNP pathology, the underlying mechanisms remain unclear. This study aimed to investigate whether eosinophilic upper airway inflammation induces hyposmia and CRSwNP in a murine model using an adoptive transfer system.

methodsTo induce eosinophilic rhinosinusitis, splenocytes, including a high proportion (over 50%) of activated eosinophils (SPLhEos), were collected from interleukin-5 transgenic mice following double intraperitoneal injections of antigens, such as ovalbumin, house dust mite, or fungus. Activated SPLhEos with corresponding antigens were then transferred into the nasal cavity of recipient mice, which were sensitized and challenged by the corresponding antigen four times per week. Olfactory function, histopathological, and computed tomography (CT) analyses were performed 2 days after the final transfer of eosinophils.

resultsHyposmia was induced significantly in mice that received SPLhEos transfer compared with healthy and allergic mice, but it did not promote morphological alteration of the paranasal sinus. Pathological analysis revealed that epithelial layer injury and metaplasia similar to polyps, with prominent eosinophil infiltration, was induced in recipient tissue. However, there was no nasal polyp development with interstitial edema that was similar to those recognized in human chronic rhinosinusitis.

conclusionsThis study supports the previously unsuspected contribution of eosinophils to CRS development in the murine model and suggests that murine-activated eosinophilic splenocytes contribute to the development of hyposmia due to more mucosal inflammation than physical airway obstruction and epithelial layer injury with convex lesions.

Indexed as

allergic rhinitischronic rhino sinusitiseosinophilhyposmianasal poly

Identifiers

PMID30764556
PMCPMC6409781
OpenAlexW2912925771

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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.