Evidence map›Paper›PMID 27714503›Full record

ArticleArchives of virology2017

IL-1β is a key cytokine that induces trypsin upregulation in the influenza virus-cytokine-trypsin cycle.

I L Indalao, T Sawabuchi, E Takahashi, H Kido

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Archives of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Deep insight into cytokine storm: from pathogenesis to treatment.Signal transduction and targeted therapy · 2025
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  3. Article
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  6. Frontiers in pharmacology · 2024
    Article
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  10. Review
  11. Article
  12. Coronavirus Precautions: Experience of High Volume Liver Transplant Institute.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2022
    Article
  13. Interleukin-6 Perpetrator of the COVID-19 Cytokine Storm.Indian journal of clinical biochemistry : IJCB · 2021
    Review
  14. Repurpose but also (nano)-reformulate! The potential role of nanomedicine in the battle against SARS-CoV2.Journal of controlled release : official journal of the Controlled Release Society · 2021
    Review
  15. The recent characteristics of influenza-related hospitalization in Japanese children.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. [Analysis of the Development Mechanism of Cytokine Storm in Severe Burn Patients Complicated with Infection].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

I L IndalaoDivision of Enzyme Chemistry, Institute for Enzyme Research, Tokushima University, Tokushima, 770-8503, Japan.
T SawabuchiDivision of Enzyme Chemistry, Institute for Enzyme Research, Tokushima University, Tokushima, 770-8503, Japan.
E TakahashiDivision of Enzyme Chemistry, Institute for Enzyme Research, Tokushima University, Tokushima, 770-8503, Japan.
H KidoDivision of Enzyme Chemistry, Institute for Enzyme Research, Tokushima University, Tokushima, 770-8503, Japan. kido@tokushima-u.ac.jp.
Tokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe influenza is characterized by a cytokine storm, and the influenza virus-cytokine-trypsin cycle is one of the important mechanisms of viral multiplication and multiple organ failure. The aim of this study was to define the key cytokine(s) responsible for trypsin upregulation. Mice were infected with influenza virus strain A/Puerto Rico/8/34 (H1N1) or treated individually or with a combination of interleukin-1β, interleukin-6, and tumor necrosis factor α. The levels of these cytokines and trypsin in the lungs were monitored. The neutralizing effects of anti-IL-1β antibodies on cytokine and trypsin expression in human A549 cells and lung inflammation in the infected mice were examined. Infection induced interleukin-1β, interleukin-6, tumor necrosis factor α, and ectopic trypsin in mouse lungs in a dose- and time-dependent manner. Intraperitoneal administration of interleukin-1β combined with other cytokines tended to upregulate trypsin and cytokine expression in the lungs, but the combination without interleukin-1β did not induce trypsin. In contrast, incubation of A549 cells with interleukin-1β alone induced both cytokines and trypsin, and anti-interleukin-1β antibody treatment abrogated these effects. Administration of the antibody in the infected mice reduced lung inflammation area. These findings suggest that IL-1β plays a key role in trypsin upregulation and has a pathological role in multiple organ failure.

Indexed as

Host-Pathogen InteractionsUp-RegulationAnimalsCell LineDisease Models, AnimalEpithelial CellsFemaleHumansInterleukin-1betaInterleukin-6LungMice, Inbred C57BLOrthomyxoviridaeOrthomyxoviridae InfectionsTrypsinTumor Necrosis Factor-alphaInterleukin-1betaInterleukin-6TrypsinTumor Necrosis Factor-alpha

Identifiers

PMID27714503
PMCPMC5225228
OpenAlexW2528286255

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.