Evidence map›Paper›PMID 26975992›Full record

ArticleInfection and immunity2016

Persisting Rickettsia typhi Causes Fatal Central Nervous System Inflammation.

Anke Osterloh, Stefanie Papp, Kristin Moderzynski, Svenja Kuehl, Ulricke Richardt, Bernhard Fleischer

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.6field-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

23 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Article
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  4. Article
  5. Cells · 2023
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  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. The neglected challenge: Vaccination against rickettsiae.PLoS neglected tropical diseases · 2020
    Review
  15. Review
  16. Rickettsial infections of the central nervous system.PLoS neglected tropical diseases · 2019
    Review
  17. Article
  18. Review
  19. Article
  20. 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

6 authors at 2 institutions in 1 country.

Anke OsterlohDepartment of Immunology, Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany osterloh@bni-hamburg.de.
Stefanie PappDepartment of Immunology, Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany.
Kristin ModerzynskiDepartment of Immunology, Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany.
Svenja KuehlDepartment of Immunology, Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany.
Ulricke RichardtDepartment of Immunology, Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany.
Bernhard FleischerInstitute for Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Bernhard Nocht Institute for Tropical Medicine · DEUniversity Medical Center Hamburg-Eppendorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rickettsioses are emerging febrile diseases caused by obligate intracellular bacteria belonging to the family Rickettsiaceae. Rickettsia typhi belongs to the typhus group (TG) of this family and is the causative agent of endemic typhus, a disease that can be fatal. In the present study, we analyzed the course of R. typhi infection in C57BL/6 RAG1(-/-) mice. Although these mice lack adaptive immunity, they developed only mild and temporary symptoms of disease and survived R. typhi infection for a long period of time. To our surprise, 3 to 4 months after infection, C57BL/6 RAG1(-/-) mice suddenly developed lethal neurological disorders. Analysis of these mice at the time of death revealed high bacterial loads, predominantly in the brain. This was accompanied by a massive expansion of microglia and by neuronal cell death. Furthermore, high numbers of infiltrating CD11b(+) macrophages were detectable in the brain. In contrast to the microglia, these cells harbored R. typhi and showed an inflammatory phenotype, as indicated by inducible nitric oxide synthase (iNOS) expression, which was not observed in the periphery. Having shown that R. typhi persists in immunocompromised mice, we finally asked whether the bacteria are also able to persist in resistant C57BL/6 and BALB/c wild-type mice. Indeed, R. typhi could be recultivated from lung, spleen, and brain tissues from both strains even up to 1 year after infection. This is the first report demonstrating persistence and reappearance of R. typhi, mainly restricted to the central nervous system in immunocompromised mice.

Indexed as

AnimalsBrainCentral Nervous System InfectionsChronic DiseaseHomeodomain ProteinsInflammationLungMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutNitric Oxide Synthase Type IIRickettsia typhiSpleenTyphus, Endemic Flea-BorneHomeodomain ProteinsNitric Oxide Synthase Type IIRAG-1 protein

Identifiers

PMID26975992
PMCPMC4862704
OpenAlexW2300127411

What OpenQuestion holds

Textmetadata
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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.