Evidence map›Paper›PMID 16861672›Full record

ArticleInfection and immunity2006

Streptococcus pneumoniae Infection aggravates experimental autoimmune encephalomyelitis via Toll-like receptor 2.

Isabel Herrmann, Markus Kellert, Hauke Schmidt, Alexander Mildner, Uwe K Hanisch, Wolfgang Brück, Marco Prinz, Roland Nau

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 25% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Article
  6. Identifying the culprits in neurological autoimmune diseases.Journal of translational autoimmunity · 2019
    Review
  7. Review
  8. Inflammatory Role of TLR-MyD88 Signaling in Multiple Sclerosis.Frontiers in molecular neuroscience · 2019
    Article
  9. Article
  10. Article
  11. Review
  12. The Autoimmune Ecology.Frontiers in immunology · 2016
    Review
  13. Article
  14. Article
  15. Article
  16. Innate immune responses in the CNS: role of toll-like receptors, mechanisms, and therapeutic opportunities in multiple sclerosis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2013
    Review
  17. Role of toll-like receptors in multiple sclerosis.American journal of clinical and experimental immunology · 2013
    Article
  18. TLR-dependent T cell activation in autoimmunity.Nature reviews. Immunology · 2011
    Review
  19. Toll-like receptors are key players in neurodegeneration.International immunopharmacology · 2011
    Review
  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

8 authors at 1 institution in 1 country.

Isabel HerrmannDepartment of Neurology, Georg August University, Robert-Koch-Str. 40, D-37075 Göttingen, Germany.
Markus Kellert
Hauke Schmidt
Alexander Mildner
Uwe K Hanisch
Wolfgang Brück
Marco Prinz
Roland Nau
University of Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The course of autoimmune inflammatory diseases of the central nervous system (CNS) can be influenced by infections. Here we assessed the disease-modulating effects of the most frequent respiratory pathogen Streptococcus pneumonia on the course of experimental autoimmune encephalomyelitis (EAE). Mice were immunized with myelin oligodendrocyte glycoprotein 35-55 (MOG(35-55)) peptide, challenged intraperitoneally with live S. pneumoniae type 3, and then treated with ceftriaxone. EAE was monitored by a clinical score for 35 days after immunization. EAE was unaltered in mice infected with S. pneumoniae 2 days before and 21 days after the first MOG(35-55) injection but was more severe in animals infected 7 days after the first MOG(35-55) injection. The antigen-driven systemic T-cell response was unaltered, and the intraspinal Th1 cytokine mRNA concentrations at the peak of disease were unchanged. The composition of CNS-infiltrating cells and subsequent tissue destruction were only slightly increased after S. pneumoniae infection. In contrast, the serum levels of tumor necrosis factor alpha and interleukin-6 and spinal interleukin-6 levels were elevated, and the expression of major histocompatibility complex class II molecules, CD80, and CD86 on splenic dendritic cells were enhanced early after infection. Serum cytokine concentrations were not elevated, and EAE was not aggravated by S. pneumoniae infection in Toll-like receptor 2 (TLR2)-deficient mice. In conclusion, infection with S. pneumoniae worsens EAE probably by elevation of proinflammatory cytokines and activation of dendritic cells in the systemic circulation via TLR2 and cross talk through the blood-brain barrier.

Indexed as

Severity of Illness IndexAnimalsCytokinesDendritic CellsEncephalomyelitis, Autoimmune, ExperimentalFemaleHumansInflammationLymphocyte ActivationMiceMice, Inbred C57BLMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinMyelin ProteinsPneumococcal InfectionsToll-Like Receptor 2CytokinesMOG protein, humanMog protein, mouseMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinMyelin ProteinsToll-Like Receptor 2

Identifiers

PMID16861672
PMCPMC1539614
OpenAlexW2108957625

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.