Evidence map›Paper›PMID 16516217›Full record

ArticleInternational journal for parasitology2006

Proliferation of Toxoplasma gondii in inflammatory macrophages in vivo is associated with diminished oxygen radical production in the host cell.

Sunder P Shrestha, Tadakimi Tomita, Louis M Weiss, Amos Orlofsky

Abstract read
In one paragraph

Article in International journal for parasitology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 23% 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

18 citing papers in PubMed, 43 citations in OpenAlex.

  1. Immunomodulatory effect of propolisOpen veterinary journal · 2024
    Article
  2. Recombinant actin-depolymerizing factor of the apicomplexanFrontiers in cellular and infection microbiology · 2022
    Article
  3. Article
  4. Functions of ROS in Macrophages and Antimicrobial Immunity.Antioxidants (Basel, Switzerland) · 2021
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Anti-Bioscience reports · 2019
    Article
  10. Article
  11. Mechanisms of Human Innate Immune Evasion byFrontiers in cellular and infection microbiology · 2019
    Review
  12. Article
  13. Contribution ofFrontiers in cellular and infection microbiology · 2017
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

4 authors at 1 institution in 1 country.

Sunder P ShresthaDepartment of Pathology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, G704, Bronx, NY 10461, USA.
Tadakimi Tomita
Louis M Weiss
Amos Orlofsky
Albert Einstein College of Medicine · US

Funding

Immunology/Pathology CoreP30AI051519 · NIAID · YESHIVA UNIVERSITY · PI GOLDSTEIN, HARRIS · 2003 to 2013
$18.6M
Toxoplasma encephalitis in AIDS:Bradyzoite RegulationsR01AI039454 · NIAID · YESHIVA UNIVERSITY · PI WEISS, LOUIS M. · 1996 to 2009
$3.1M
Regulation of Macrophage Cell Death by Toxoplasma gondiiR01AI055358 · NIAID · ALBERT EINSTEIN COL OF MED YESHIVA UNIV · PI ORLOFSKY, AMOS Z · 2004 to 2008
$2.0M
NIAID NIH HHS AI-39454NIAID NIH HHS AI-51519NIAID NIH HHS AI-55358NIAID NIH HHS P30 AI051519NIAID NIH HHS R01 AI039454NIAID NIH HHS R01 AI055358
6 · The paper itself

Abstract

While reactive oxygen species (ROS) can kill Toxoplasma gondii in vitro the role these molecules play in vivo is not known. We used a flow cytometry-based assay to investigate the relationship between intracellular infection and ROS production during acute peritoneal toxoplasmosis in mice. A distinct population of ROS(+) inflammatory macrophages, detected by the oxidation of hydroethidine, was observed to increase progressively in frequency during the course of infection, and to be inversely correlated with the degree of cell parasitization. These data imply that either intracellular parasites inhibit ROS synthesis or, alternatively, ROS-producing cells contain anti-Toxoplasma activity. The latter interpretation was supported by the finding that uninfected ROS-producing inflammatory macrophages were resistant to infection in vivo. However, in the same animals, ROS-producing macrophages that had previously been parasitized could readily be infected with additional parasites, suggesting that the difference in ROS production between highly infected and less infected cells was not due to ROS-associated killing of parasites within these cells. In addition, macrophages infected with T. gondii in vitro and then briefly transferred to acutely infected mice upregulated ROS production in a manner that was again inversely correlated with the degree of intracellular parasitization. Taken together, these findings suggest that both ROS-associated anti-Toxoplasma activity and parasite-driven inhibition of ROS production underlie the observed pattern of ROS production. ROS function and parasite evasion of this function may contribute significantly to the balance between host defense and disease progression during acute infection.

Indexed as

Acute DiseaseAnimalsDisease Models, AnimalFemaleHost-Parasite InteractionsMacrophages, PeritonealMiceMice, Inbred C57BLReactive Oxygen SpeciesToxoplasmaToxoplasmosis, AnimalUp-RegulationReactive Oxygen Species

Identifiers

PMID16516217
PMCPMC3109651
OpenAlexW2074043231

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.