Evidence map›Paper›PMID 29695841›Full record

ArticleMucosal immunology2018

Pulmonary Regnase-1 orchestrates the interplay of epithelium and adaptive immune systems to protect against pneumonia.

Yoshinari Nakatsuka, Alexis Vandenbon, Takashi Mino, Masanori Yoshinaga, Takuya Uehata, Xiaotong Cui, Ayuko Sato, Tohru Tsujimura, Yutaka Suzuki, Atsuyasu Sato and 5 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

12 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  5. RNA Metabolism Governs Immune Function and Response.Advances in experimental medicine and biology · 2024
    Review
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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

15 authors at 5 institutions in 1 country.

Yoshinari NakatsukaLaboratory of Infection and Prevention, Department of Virus Research, Institute for Frontier Life and Medical Sciences, Kyoto University, 253 Shogoin Kawara-cho, Sakyo-ku, Kyoto, 606-8507, Japan.
Alexis VandenbonLaboratory of Infection and Prevention, Department of Virus Research, Institute for Frontier Life and Medical Sciences, Kyoto University, 253 Shogoin Kawara-cho, Sakyo-ku, Kyoto, 606-8507, Japan.
Takashi MinoLaboratory of Infection and Prevention, Department of Virus Research, Institute for Frontier Life and Medical Sciences, Kyoto University, 253 Shogoin Kawara-cho, Sakyo-ku, Kyoto, 606-8507, Japan.
Masanori YoshinagaLaboratory of Infection and Prevention, Department of Virus Research, Institute for Frontier Life and Medical Sciences, Kyoto University, 253 Shogoin Kawara-cho, Sakyo-ku, Kyoto, 606-8507, Japan.
Takuya UehataLaboratory of Infection and Prevention, Department of Virus Research, Institute for Frontier Life and Medical Sciences, Kyoto University, 253 Shogoin Kawara-cho, Sakyo-ku, Kyoto, 606-8507, Japan.
Xiaotong CuiLaboratory of Infection and Prevention, Department of Virus Research, Institute for Frontier Life and Medical Sciences, Kyoto University, 253 Shogoin Kawara-cho, Sakyo-ku, Kyoto, 606-8507, Japan.
Ayuko SatoDepartment of Pathology, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo, 663-8501, Japan.
Tohru TsujimuraDepartment of Pathology, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo, 663-8501, Japan.
Yutaka SuzukiLaboratory of Functional Genomics, Department of Medical Genome Sciences, Graduate School of Frontier Sciences, The University of Tokyo, 5-1-5 Kashiwanoha, Kashiwa-shi, Chiba, 277-8562, Japan.
Atsuyasu SatoDepartment of Respiratory Medicine, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, 606-8507, Japan.
Tomohiro HandaDepartment of Respiratory Medicine, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, 606-8507, Japan.
Kazuo ChinDepartment of Respiratory Care and Sleep Medicine, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-Ku, Kyoto, 606-8507, Japan.
Teiji SawaDepartment of Anesthesiology, Kyoto Prefectural University of Medicine, Kawaramachi Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan.
Toyohiro HiraiDepartment of Respiratory Medicine, Graduate School of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, 606-8507, Japan.
Osamu TakeuchiLaboratory of Infection and Prevention, Department of Virus Research, Institute for Frontier Life and Medical Sciences, Kyoto University, 253 Shogoin Kawara-cho, Sakyo-ku, Kyoto, 606-8507, Japan. otake@virus.kyoto-u.ac.jp.
Kyoto University · JPJapan Agency for Medical Research and Development · JPHyogo Medical University · JPKyoto Prefectural University of Medicine · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inhaled pathogens including Pseudomonas aeruginosa initially encounter airway epithelial cells (AECs), which are poised to evoke cell-intrinsic innate defense, affecting second tier of hematopoietic cell-mediated immune reaction. However, it is largely unknown how pulmonary immune responses mediated by a variety of immune cells are coordinated. Here we show that Regnase-1, an endoribonuclease expressed in AECs and immune cells, plays an essential role in coordinating innate responses and adaptive immunity against P. aeruginosa infection. Intratracheal treatment of mice with heat-killed P. aeruginosa resulted in prolonged disappearance of Regnase-1 consistent with sustained expression of Regnase-1 target inflammatory genes, whereas the transcription factor NF-κB was only transiently activated. AEC-specific deletion of Regnase-1 not only augmented innate defenses against P. aeruginosa but also enhanced secretion of Pseudomonas-specific IgA and Th17 accumulation in the lung, culminating in conferring significant resistance against P. aeruginosa re-infection in vivo. Although Regnase-1 directly controls distinct sets of genes in each of AECs and T cells, degradation of Regnase-1 in both cell types is beneficial for maximizing acquired immune responses. Collectively, these results demonstrate that Regnase-1 orchestrates AEC-mediated and immune cell-mediated host defense against pulmonary bacterial infection.

Indexed as

Adaptive ImmunityAnimalsAntibodies, BacterialImmunity, InnateImmunoglobulin ALungLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutNF-kappa BPneumonia, BacterialPseudomonas aeruginosaPseudomonas InfectionsRespiratory MucosaRibonucleasesAntibodies, BacterialImmunoglobulin ANF-kappa BRibonucleasesZc3h12a protein, mouse

Identifiers

PMID29695841
OpenAlexW2800887909

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.