Evidence map›Paper›PMID 34167455›Full record

ArticleMolecular medicine (Cambridge, Mass.)2021

Spatiotemporally specific roles of TLR4, TNF, and IL-17A in murine endotoxin-induced inflammation inferred from analysis of dynamic networks.

Ruben Zamora, Sangeeta Chavan, Theodoros Zanos, Richard L Simmons, Timothy R Billiar, Yoram Vodovotz

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

16 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  7. Gut microbiota in insulin resistance: a bibliometric analysis.Journal of diabetes and metabolic disorders · 2024
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  14. What's next for computational systems biology?Frontiers in systems biology · 2023
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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

6 authors.

Ruben ZamoraDepartment of Surgery, University of Pittsburgh, Starzl Biomedical Sciences Tower, 200 Lothrop St., Pittsburgh, PA, 15213, USA.ORCID 0000-0003-3882-9087
Sangeeta ChavanInstitute of Bioelectronic Medicine, The Feinstein Institutes for Medical Research, Manhasset, NY, USA.
Theodoros ZanosInstitute of Bioelectronic Medicine, The Feinstein Institutes for Medical Research, Manhasset, NY, USA.
Richard L SimmonsDepartment of Surgery, University of Pittsburgh, Starzl Biomedical Sciences Tower, 200 Lothrop St., Pittsburgh, PA, 15213, USA.
Timothy R BilliarDepartment of Surgery, University of Pittsburgh, Starzl Biomedical Sciences Tower, 200 Lothrop St., Pittsburgh, PA, 15213, USA.
Yoram VodovotzDepartment of Surgery, University of Pittsburgh, Starzl Biomedical Sciences Tower, 200 Lothrop St., Pittsburgh, PA, 15213, USA. vodovotzy@upmc.edu.ORCID 0000-0002-4389-8768

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBacterial lipopolysaccharide (LPS) induces a multi-organ, Toll-like receptor 4 (TLR4)-dependent acute inflammatory response.

methodsUsing network analysis, we defined the spatiotemporal dynamics of 20, LPS-induced, protein-level inflammatory mediators over 0-48 h in the heart, gut, lung, liver, spleen, kidney, and systemic circulation, in both C57BL/6 (wild-type) and TLR4-null mice.

resultsDynamic Network Analysis suggested that inflammation in the heart is most dependent on TLR4, followed by the liver, kidney, plasma, gut, lung, and spleen, and raises the possibility of non-TLR4 LPS signaling pathways at defined time points in the gut, lung, and spleen. Insights from computational analyses suggest an early role for TLR4-dependent tumor necrosis factor in coordinating multiple signaling pathways in the heart, giving way to later interleukin-17A-possibly derived from pathogenic Th17 cells and effector/memory T cells-in the spleen and blood.

conclusionsWe have derived novel, systems-level insights regarding the spatiotemporal evolution acute inflammation.

Indexed as

Disease SusceptibilityAnimalsBiomarkersComputational BiologyCytokinesDisease Models, AnimalEndotoxinsInflammationInflammation MediatorsInterleukin-17MaleMiceMice, TransgenicToll-Like Receptor 4Tumor Necrosis Factor-alphaBiomarkersCytokinesEndotoxinsInflammation MediatorsInterleukin-17Toll-Like Receptor 4Tumor Necrosis Factor-alphaChemokinesCytokinesDynamic Network AnalysisEndotoxemiaEndotoxinLipopolysaccharidePrincipal Component AnalysisTLR4

Identifiers

PMID34167455
PMCPMC8223370

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Registered trials

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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.