Evidence map›Paper›PMID 30455472›Full record

ArticleNature microbiology2019

Pulmonary phagocyte-derived NPY controls the pathology of severe influenza virus infection.

Seiki Fujiwara, Midori Hoshizaki, Yu Ichida, Dennis Lex, Etsushi Kuroda, Ken J Ishii, Shigeyuki Magi, Mariko Okada, Hiroyuki Takao, Masahiro Gandou and 10 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 31% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  5. Cytokines reprogram airway sensory neurons in asthma.bioRxiv : the preprint server for biology · 2024
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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

20 authors at 10 institutions in 5 countries.

Seiki FujiwaraLaboratory of Regulation for Intractable Infectious Diseases, Center for Vaccine and Adjuvant Research (CVAR), National Institutes of Biomedical Innovation Health and Nutrition (NIBIOHN), Osaka, Japan.
Midori HoshizakiLaboratory of Regulation for Intractable Infectious Diseases, Center for Vaccine and Adjuvant Research (CVAR), National Institutes of Biomedical Innovation Health and Nutrition (NIBIOHN), Osaka, Japan.
Yu IchidaLaboratory of Regulation for Intractable Infectious Diseases, Center for Vaccine and Adjuvant Research (CVAR), National Institutes of Biomedical Innovation Health and Nutrition (NIBIOHN), Osaka, Japan.
Dennis LexInstitute of Pharmacology and Toxicology, Medical Faculty, RWTH Aachen University, Aachen, Germany.
Etsushi KurodaLaboratory of Adjuvant Innovation, Center for Vaccine and Adjuvant Research (CVAR), National Institutes of Biomedical Innovation Health and Nutrition (NIBIOHN), Osaka, Japan.
Ken J IshiiLaboratory of Adjuvant Innovation, Center for Vaccine and Adjuvant Research (CVAR), National Institutes of Biomedical Innovation Health and Nutrition (NIBIOHN), Osaka, Japan.ORCID http://orcid.org/0000-0002-6728-3872
Shigeyuki MagiLaboratory of Cell Systems, Institute for Protein Research, Osaka University, Osaka, Japan.
Mariko OkadaLaboratory of Cell Systems, Institute for Protein Research, Osaka University, Osaka, Japan.
Hiroyuki TakaoLaboratory of Regulation for Intractable Infectious Diseases, Center for Vaccine and Adjuvant Research (CVAR), National Institutes of Biomedical Innovation Health and Nutrition (NIBIOHN), Osaka, Japan.
Masahiro GandouLaboratory of Regulation for Intractable Infectious Diseases, Center for Vaccine and Adjuvant Research (CVAR), National Institutes of Biomedical Innovation Health and Nutrition (NIBIOHN), Osaka, Japan.
Hirotaka ImaiLaboratory of Regulation for Intractable Infectious Diseases, Center for Vaccine and Adjuvant Research (CVAR), National Institutes of Biomedical Innovation Health and Nutrition (NIBIOHN), Osaka, Japan.
Ryujiro HaraLaboratory of Regulation for Intractable Infectious Diseases, Center for Vaccine and Adjuvant Research (CVAR), National Institutes of Biomedical Innovation Health and Nutrition (NIBIOHN), Osaka, Japan.
Herbert HerzogNeuroscience Division, Garvan Institute of Medical Research, Sydney, New South Wales, Australia.
Akihiko YoshimuraDepartment of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan.
Hitoshi OkamuraLaboratory of Molecular Brain Science, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan.
Josef M PenningerInstitute of Molecular Biotechnology in the Austrian Academy of Sciences, Vienna, Austria.
Arthur S SlutskyKeenan Research Center, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ontario, Canada.
Stefan UhligInstitute of Pharmacology and Toxicology, Medical Faculty, RWTH Aachen University, Aachen, Germany.
Keiji KubaDepartment of Biochemistry and Metabolic Science, Akita University Graduate School of Medicine, Akita, Japan.
Yumiko ImaiLaboratory of Regulation for Intractable Infectious Diseases, Center for Vaccine and Adjuvant Research (CVAR), National Institutes of Biomedical Innovation Health and Nutrition (NIBIOHN), Osaka, Japan. y-imai@nibiohn.go.jp.ORCID http://orcid.org/0000-0003-4615-4833
National Institute of Biomedical Innovation, Health and Nutrition · JPRWTH Aachen University · DEAkita University · JPGarvan Institute of Medical Research · AUInstitute of Molecular Biotechnology · ATKeio University · JPKyoto University · JPProtein Research Foundation · JPRIKEN Center for Integrative Medical Sciences · JPSt. Michael's Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Crosstalk between the autonomic nervous system and the immune system by means of the sympathetic and parasympathetic pathways is a critical process in host defence. Activation of the sympathetic nervous system results in the release of catecholamines as well as neuropeptide Y (NPY). Here, we investigated whether phagocytes are capable of the de novo production of NPY, as has been described for catecholamines. We show that the synthesis of NPY and its Y1 receptor (Y1R) is increased in phagocytes in lungs following severe influenza virus infection. The genetic deletion of Npy or Y1r specifically in phagocytes greatly improves the pathology of severe influenza virus infection, which is characterized by excessive virus replication and pulmonary inflammation. Mechanistically, it is the induction of suppressor of cytokine signalling 3 (SOCS3) via NPY-Y1R activation that is responsible for impaired antiviral response and promoting pro-inflammatory cytokine production, thereby enhancing the pathology of influenza virus infection. Thus, direct regulation of the NPY-Y1R-SOCS3 pathway on phagocytes may act as a fine-tuner of an innate immune response to virus infection, which could be a therapeutic target for lethal influenza virus infection.

Indexed as

AnimalsCytokinesGene DeletionHost-Pathogen InteractionsInfluenza A virusLungMiceNeuropeptide YOrthomyxoviridae InfectionsPhagocytesReceptors, Neuropeptide YSignal TransductionSuppressor of Cytokine Signaling 3 ProteinSurvival AnalysisTranscription, GeneticVirus ReplicationCytokinesNeuropeptide Yneuropeptide Y-Y1 receptorReceptors, Neuropeptide YSocs3 protein, mouseSuppressor of Cytokine Signaling 3 Protein

Identifiers

PMID30455472
OpenAlexW2901007087

What OpenQuestion holds

Textmetadata
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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.