Evidence map›Paper›PMID 36710253›Full record

SynthesisWIREs mechanisms of disease

Interleukin-17 as a spatiotemporal bridge from acute to chronic inflammation: Novel insights from computational modeling.

Ashti M Shah, Ruben Zamora, Yoram Vodovotz

Open access · greenAbstract readSystematic Review
In one paragraph

Synthesis in WIREs mechanisms of disease. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. What's next for computational systems biology?Frontiers in systems biology · 2023
    Review
  7. Review
  8. Review
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

3 authors at 1 institution in 1 country.

Ashti M ShahPhysician Scientist Training Program, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.ORCID 0000-0001-8990-9509
Ruben ZamoraDepartment of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.ORCID 0000-0003-3882-9087
Yoram VodovotzDepartment of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.ORCID 0000-0002-4389-8768
University of Pittsburgh · US

Funding

Multi-Center Group to Study Acute Liver Failure in ChildU01DK072146 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SQUIRES, ROBERT H · 2005 to 2014
$23.2M
Regulation of Intestinal Mucosal Injury & Repair After Trauma/Hemorrhagic ShockP50GM053789 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BILLIAR, TIMOTHY R · 1997 to 2013
$18.0M
Surgery triggered immune response and liver metastasesR01CA214865 · NCI · UNIVERSITY OF VIRGINIA · PI Allan Tsung · 2018 to 2026
$3.4M
Modeling Brainstem Inflammation's Role in Systemic Dysfunction during SepsisU01EB021960 · NIBIB · CASE WESTERN RESERVE UNIVERSITY · PI DICK, THOMAS E · 2017 to 2020
$2.6M
A Biohybrid Device for Regulating Inflammation in SepsisR01GM107231 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GERLACH, JOERG C., VODOVOTZ, YORAM · 2015 to 2017
$1.0M
NCI NIH HHS R01 CA214865NIBIB NIH HHS U01 EB021960NIDDK NIH HHS U01 DK072146NIGMS NIH HHS P50 GM053789NIGMS NIH HHS R01 GM107231
6 · The paper itself

Abstract

A systematic review of several acute inflammatory diseases ranging from sepsis and trauma/hemorrhagic shock to the relevant pathology of the decade, COVID-19, points to the cytokine interleukin (IL)-17A as being centrally involved in the propagation of inflammation. We summarize the role of IL-17A in acute inflammation, leveraging insights made possible by biological network analysis and novel computational methodologies aimed at defining the spatiotemporal spread of inflammation in both experimental animal models and humans. These studies implicate IL-17A in the cross-tissue spread of inflammation, a process that appears to be in part regulated through neural mechanisms. Although acute inflammatory diseases are currently considered distinct from chronic inflammatory pathologies, we suggest that chronic inflammation may represent repeated, cyclical episodes of acute inflammation driven by mechanisms involving IL-17A. Thus, insights from computational modeling of acute inflammatory diseases may improve diagnosis and treatment of chronic inflammation; in turn, therapeutics developed for chronic/autoimmune disease may be of benefit in acute inflammation. This article is categorized under: Immune System Diseases > Computational Models.

Indexed as

COVID-19Interleukin-17AnimalsChronic DiseaseComputer SimulationHumansInflammationInterleukin-17acute inflammationcomputational modelingIL-17A

Identifiers

PMID36710253
PMCPMC10176872
OpenAlexW4318543026

What OpenQuestion holds

Textmetadata
LicenceTDM
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.