Evidence map›Paper›PMID 27088594›Full record

ArticlePloS one2016

Impact of Histone H1 on the Progression of Allergic Rhinitis and Its Suppression by Neutralizing Antibody in Mice.

Toshiaki Nakano, Rikiya Kamei, Takashi Fujimura, Yuki Takaoka, Ayane Hori, Chia-Yun Lai, Kuei-Chen Chiang, Yayoi Shimada, Naoya Ohmori, Takeshi Goto and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Linker Histone in Diseases.International journal of biological sciences · 2017
    Review
  5. 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

14 authors at 4 institutions in 2 countries.

Toshiaki NakanoGraduate Institute of Clinical Medical Sciences, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Rikiya KameiDepartment of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University, Higashi-Hiroshima, Japan.
Takashi FujimuraDepartment of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University, Higashi-Hiroshima, Japan.
Yuki TakaokaLiver Transplantation Center and Division of Transplant Immunology, Institute for Translational Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan.
Ayane HoriDepartment of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University, Higashi-Hiroshima, Japan.
Chia-Yun LaiLiver Transplantation Center and Division of Transplant Immunology, Institute for Translational Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan.
Kuei-Chen ChiangKazusa Institute for Drug Discovery, Josai International University, Kisarazu, Japan.
Yayoi ShimadaKazusa Institute for Drug Discovery, Josai International University, Kisarazu, Japan.
Naoya OhmoriKazusa Institute for Drug Discovery, Josai International University, Kisarazu, Japan.
Takeshi GotoKazusa Institute for Drug Discovery, Josai International University, Kisarazu, Japan.
Kazuhisa OnoDepartment of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University, Higashi-Hiroshima, Japan.
Chao-Long ChenLiver Transplantation Center and Division of Transplant Immunology, Institute for Translational Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan.
Shigeru GotoLiver Transplantation Center and Division of Transplant Immunology, Institute for Translational Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan.
Seiji KawamotoDepartment of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University, Higashi-Hiroshima, Japan.
Hiroshima University · JPJosai International University · JPKaohsiung Chang Gung Memorial Hospital · TWHiroshima Institute of Technology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nuclear antigens are known to trigger off innate and adaptive immune responses. Recent studies have found that the complex of nucleic acids and core histones that are derived from damaged cells may regulate allergic responses. However, no fundamental study has been performed concerning the role of linker histone H1 in mast cell-mediated type I hyperreactivity. In this study, we explored the impact of histone H1 on mast cell-mediated allergic responses both in vitro and in vivo. In the course of a bona-fide experimental allergen sensitization model upon co-injection with alum adjuvant, ovalbumin (OVA), but not PBS, induced elevated levels of circulating histone H1. Intranasal challenge with histone H1 to OVA/alum- (but not PBS/alum)-sensitized mice induced significantly severer symptoms of allergic rhinitis than those in mice sensitized and challenged with OVA. A monoclonal antibody against histone H1 not only suppressed mast cell degranulation, but also ameliorated OVA-induced nasal hyperreactivity and IgE-mediated passive cutaneous anaphylaxis. Our present data suggest that nuclear histone H1 represents an alarmin-like endogenous mediator acting on mast cells, and that its blockage has a therapeutic potential for mast cell-mediated type I hyperreactivity.

Indexed as

AllergensAnimalsAntibodies, NeutralizingBlotting, WesternDisease Models, AnimalDisease ProgressionFemaleHistonesImmunoenzyme TechniquesImmunoglobulin EMaleMast CellsMiceMice, Inbred BALB COvalbuminPassive Cutaneous AnaphylaxisAllergensAntibodies, NeutralizingHistonesImmunoglobulin EOvalbuminPeptide Fragments

Identifiers

PMID27088594
PMCPMC4835108
OpenAlexW2342289673

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.