Evidence map›Paper›PMID 26913029›Full record

ArticleFrontiers in microbiology2016

One Episode of Self-Resolving Plasmodium yoelii Infection Transiently Exacerbates Chronic Mycobacterium tuberculosis Infection.

Jannike Blank, Lars Eggers, Jochen Behrends, Thomas Jacobs, Bianca E Schneider

Open access · goldAbstract read
In one paragraph

Article in Frontiers in microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.8field-weighted citation impact, top 13% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Review
  3. Lessons Learned for Pathogenesis, Immunology, and Disease of Erythrocytic Parasites:Frontiers in cellular and infection microbiology · 2021
    Review
  4. Article
  5. Sex differences in tuberculosis.Seminars in immunopathology · 2019
    Review
  6. Article
  7. 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

5 authors at 2 institutions in 1 country.

Jannike BlankDivision of Coinfection, Priority Research Area Infections, Research Center Borstel Borstel, Germany.
Lars EggersDivision of Coinfection, Priority Research Area Infections, Research Center Borstel Borstel, Germany.
Jochen BehrendsFluorescence Cytometry Core Facility, Research Center Borstel Borstel, Germany.
Thomas JacobsDepartment of Immunology, Bernhard Nocht Institute for Tropical Medicine Hamburg, Germany.
Bianca E SchneiderDivision of Coinfection, Priority Research Area Infections, Research Center Borstel Borstel, Germany.
Research Center Borstel - Leibniz Lung Center · DEBernhard Nocht Institute for Tropical Medicine · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malaria and tuberculosis (Tb) are two of the main causes of death from infectious diseases globally. The pathogenic agents, Plasmodium parasites and Mycobacterium tuberculosis, are co-endemic in many regions in the world, however, compared to other co-infections like HIV/Tb or helminth/Tb, malaria/Tb has been given less attention both in clinical and immunological studies. Due to the lack of sufficient human data, the impact of malaria on Tb and vice versa is difficult to estimate but co-infections are likely to occur very frequently. Due to its immunomodulatory properties malaria might be an underestimated risk factor for latent or active Tb patients particularly in high-endemic malaria settings were people experience reinfections very frequently. In the present study, we used the non-lethal strain of Plasmodium yoelii to investigate, how one episode of self-resolving malaria impact on a chronic M. tuberculosis infection. P. yoelii co-infection resulted in exacerbation of Tb disease as demonstrated by increased pathology and cellular infiltration of the lungs which coincided with elevated levels of pro- and anti-inflammatory mediators. T cell responses were not impaired in co-infected mice but enhanced and likely contributed to increased cytokine production. We found a slight but statistically significant increase in M. tuberculosis burden in co-infected animals and increased lung CFU was positively correlated with elevated levels of TNFα but not IL-10. Infection with P. yoelii induced the recruitment of a CD11c(+) population into lungs and spleens of M. tuberculosis infected mice. CD11c(+) cells isolated from P. yoelii infected spleens promoted survival and growth of M. tuberculosis in vitro. 170 days after P. yoelii infection changes in immunopathology and cellular immune responses were no longer apparent while M. tuberculosis numbers were still slightly higher in lungs, but not in spleens of co-infected mice. In conclusion, one episode of P. yoelii co-infection transiently exacerbated disease severity but had no long-term consequences on disease progression and survival of M. tuberculosis infected mice.

Indexed as

co-infectionmouse modelMycobacterium tuberculosisPlasmodium yoelii malariatuberculosis

Identifiers

PMID26913029
PMCPMC4753732
OpenAlexW2286548552

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.