Evidence map›Paper›PMID 31385572›Full record

ArticleeLife2019

IFN-mediated negative feedback supports bacteria class-specific macrophage inflammatory responses.

Rachel A Gottschalk, Michael G Dorrington, Bhaskar Dutta, Kathleen S Krauss, Andrew J Martins, Stefan Uderhardt, Waipan Chan, John S Tsang, Parizad Torabi-Parizi, Iain Dc Fraser and 1 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. The Regulatory Mechanisms of Treponema pallidum Enolase on Macrophages: From Enzymatic Activity to Signal Transduction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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  12. Regulation of myeloid-cell activation.Current opinion in immunology · 2021
    Review
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  15. Article
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  17. Article
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

11 authors at 2 institutions in 1 country.

Rachel A Gottschalk *Lymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, United States.ORCID 0000-0002-5248-8816
Michael G Dorrington *Signaling Systems Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, United States.
Bhaskar DuttaLymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, United States.
Kathleen S KraussLymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, United States.
Andrew J MartinsSystems Genomics and Bioinformatics Unit, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, United States.
Stefan UderhardtLymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, United States.
Waipan ChanLymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, United States.
John S TsangSystems Genomics and Bioinformatics Unit, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, United States.
Parizad Torabi-PariziCritical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, United States.
Iain Dc FraserSignaling Systems Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, United States.
Ronald N GermainLymphocyte Biology Section, Laboratory of Immune System Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, United States.ORCID 0000-0003-1495-9143
National Institutes of Health · USNational Institutes of Health Clinical Center · US

Funding

National Institute of Allergy and Infectious Diseases Intramural Research Program
6 · The paper itself

Abstract

Despite existing evidence for tuning of innate immunity to different classes of bacteria, the molecular mechanisms used by macrophages to tailor inflammatory responses to specific pathogens remain incompletely defined. By stimulating mouse macrophages with a titration matrix of TLR ligand pairs, we identified distinct stimulus requirements for activating and inhibitory events that evoked diverse cytokine production dynamics. These regulatory events were linked to patterns of inflammatory responses that distinguished between Gram-positive and Gram-negative bacteria, both in vitro and after in vivo lung infection. Stimulation beyond a TLR4 threshold and Gram-negative bacteria-induced responses were characterized by a rapid type I IFN-dependent decline in inflammatory cytokine production, independent of IL-10, whereas inflammatory responses to Gram-positive species were more sustained due to the absence of this IFN-dependent regulation. Thus, disparate triggering of a cytokine negative feedback loop promotes tuning of macrophage responses in a bacteria class-specific manner and provides context-dependent regulation of inflammation dynamics.

Indexed as

Feedback, PhysiologicalAnimalsCells, CulturedCytokinesDisease Models, AnimalGram-Negative BacteriaGram-Positive BacteriaInterferon Type IMacrophagesMice, Inbred C57BLPneumonia, BacterialCytokinesInterferon Type Icomputational biologyimmunologyinflammationmacrophagemousenegative feedbacksignal integrationsystems biologytype I IFN

Identifiers

PMID31385572
PMCPMC6684266
OpenAlexW2966249001

What OpenQuestion holds

Textmetadata
LicenceCC0
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.