Evidence map›Paper›PMID 19549875›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Modeling the immune rheostat of macrophages in the lung in response to infection.

Judy Day, Avner Friedman, Larry S Schlesinger

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

64 citing papers in PubMed, 136 citations in OpenAlex.

  1. Review
  2. Review
  3. Evolution and host-specific adaptation ofScience (New York, N.Y.) · 2024
    Article
  4. Article
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  11. Host defense mechanisms against Mycobacterium tuberculosis.Cellular and molecular life sciences : CMLS · 2020
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Cardiac macrophage biology in the steady-state heart, the aging heart, and following myocardial infarction.Translational research : the journal of laboratory and clinical medicine · 2018
    Review
  20. Frontiers in cellular and infection microbiology · 2018
    Article

4 more citing papers are in PubMed but not listed here.

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 2 institutions in 3 countries.

Judy DayMathematical Biosciences Institute, Ohio State University, Columbus, OH 43210, USA.
Avner Friedman
Larry S Schlesinger
Interface (United Kingdom) · GBThe Ohio State University · US

Funding

University of Iowa Clinical and Translational Science Program (TL1)UL1RR025755 · NCRR · OHIO STATE UNIVERSITY · PI JACKSON, REBECCA D · 2008 to 2011
$26.3M
TB and Innate Immune Regulation of Lung MacrophagesR01AI059639 · NIAID · OHIO STATE UNIVERSITY · PI SCHLESINGER, LARRY S. · 2005 to 2016
$3.2M
TB and Innate Immune Regulation of Lung MacrophagesR21AI059639 · NIAID · OHIO STATE UNIVERSITY · PI SCHLESINGER, LARRY S. · 2004 to 2004
$299k
NCRR NIH HHS UL1 RR025755NIAID NIH HHS AI059639NIAID NIH HHS R01 AI059639NIAID NIH HHS R21 AI059639
6 · The paper itself

Abstract

In the lung, alternatively activated macrophages (AAM) form the first line of defense against microbial infection. Due to the highly regulated nature of AAM, the lung can be considered as an immunosuppressive organ for respiratory pathogens. However, as infection progresses in the lung, another population of macrophages, known as classically activated macrophages (CAM) enters; these cells are typically activated by IFN-gamma. CAM are far more effective than AAM in clearing the microbial load, producing proinflammatory cytokines and antimicrobial defense mechanisms necessary to mount an adequate immune response. Here, we are concerned with determining the first time when the population of CAM becomes more dominant than the population of AAM. This proposed "switching time" is explored in the context of Mycobacterium tuberculosis (MTb) infection. We have developed a mathematical model that describes the interactions among cells, bacteria, and cytokines involved in the activation of both AAM and CAM. The model, based on a system of differential equations, represents a useful tool to analyze strategies for reducing the switching time, and to generate hypotheses for experimental testing.

Indexed as

Models, ImmunologicalComputer SimulationCytokinesDendritic CellsExtracellular SpaceImmune SystemIntracellular SpaceLungMacrophage ActivationMacrophages, AlveolarMycobacterium tuberculosisReproducibility of ResultsTime FactorsT-LymphocytesCytokines

Identifiers

PMID19549875
PMCPMC2708732
OpenAlexW2047420973

What OpenQuestion holds

Textmetadata
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.