Evidence map›Paper›PMID 27878831›Full record

ArticleAllergy2017

IκBNS induces Muc5ac expression in epithelial cells and causes airway hyper-responsiveness in murine asthma models.

M Yokota, T Tamachi, Y Yokoyama, Y Maezawa, H Takatori, A Suto, K Suzuki, K Hirose, K Takeda, H Nakajima

Abstract read
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In one paragraph

Article in Allergy, 2017. 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
1.4field-weighted citation impact, top 18% 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, 19 citations in OpenAlex.

  1. Regulation and Function of the Atypical IκBs-Bcl-3, IκBEuropean journal of immunology · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

M YokotaDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
T TamachiDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Y YokoyamaDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Y MaezawaDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
H TakatoriDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
A SutoDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
K SuzukiDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
K HiroseDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
K TakedaLaboratory of Immune Regulation, Department of Microbiology and Immunology, Graduate School of Medicine and Laboratory of Mucosal Immunology, WPI Immunology Frontier Research Center, Osaka University, Osaka, Japan.
H NakajimaDepartment of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Chiba University · JPOsaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn allergic asthma, environmental allergens including house dust mite (HDM) trigger pattern recognition receptors and activate downstream signaling pathways including NF-κB pathways not only in immune cells but also in airway epithelial cells. Recent studies have shown that NF-κB activation is regulated positively or negatively depending on the cellular context by IκBNS (encoded by the gene Nfkbid), one of atypical IκB proteins, in the nucleus. Therefore, we hypothesized that IκBNS expressed in immune cells or epithelial cells is involved in the regulation of asthmatic responses.

aimTo determine the roles of IκBNS in HDM-induced asthmatic responses.

methodsRoles of IκBNS in HDM-induced airway inflammation and airway hyper-responsiveness (AHR) were examined by using IκBNS-deficient (Nfkbid

resultsHouse dust mite-induced airway inflammation and AHR were exacerbated in mice lacking IκBNS in hematopoietic cells. In contrast, HDM-induced airway inflammation was exacerbated, but AHR was attenuated in mice lacking IκBNS in nonhematopoietic cells. The induction of Muc5ac, a representative mucin in asthmatic airways, was reduced in Nfkbid

conclusionIκBNS is involved in inducing Muc5ac expression in lung epithelial cells and causing AHR in HDM-induced asthma models.

Indexed as

Gene Expression RegulationAllergensAnimalsAsthmaBlood CellsCytokinesDermatophagoides pteronyssinusDisease Models, AnimalDisease ProgressionI-kappa B ProteinsInflammation MediatorsMiceMice, KnockoutMucin 5ACMucusPromoter Regions, GeneticAllergensCytokinesI-kappa B ProteinsInflammation MediatorsMuc5ac protein, mouseMucin 5ACairway hyper-responsivenessasthmaIκBNSMuc5ac

Identifiers

PMID27878831
OpenAlexW2547794794

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.