Evidence map›Paper›PMID 17571163›Full record

ArticleThe Journal of clinical investigation2007

TRAIL limits excessive host immune responses in bacterial meningitis.

Olaf Hoffmann, Josef Priller, Timour Prozorovski, Ulf Schulze-Topphoff, Nevena Baeva, Jan D Lunemann, Orhan Aktas, Cordula Mahrhofer, Sarah Stricker, Frauke Zipp and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.2field-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

30 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
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  3. Review
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  5. Review
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  7. Distinct roles of TNF-related apoptosis-inducing ligand (TRAIL) in viral and bacterial infections: from pathogenesis to pathogen clearance.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016
    Review
  8. Review
  9. Article
  10. Airway Inflammation after Bronchial Thermoplasty for Severe Asthma.Annals of the American Thoracic Society · 2015
    Observational
  11. Article
  12. Article
  13. Article
  14. Article
  15. Soluble TRAIL in normal pregnancy and acute pyelonephritis: a potential explanation for the susceptibility of pregnant women to microbial products and infection.The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2013
    Article
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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

11 authors at 2 institutions in 2 countries.

Olaf HoffmannDepartment of Neurology, Laboratory of Molecular Psychiatry, Charité Universitätsmedizin Berlin, Berlin, Germany.
Josef Priller
Timour Prozorovski
Ulf Schulze-Topphoff
Nevena Baeva
Jan D Lunemann
Orhan Aktas
Cordula Mahrhofer
Sarah Stricker
Frauke Zipp
Joerg R Weber
Institute of Neuroimmunology of the Slovak Academy of Sciences · SKLaboratory of Molecular Genetics · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apart from potential roles in anti-tumor surveillance, the TNF-related apoptosis-inducing ligand (TRAIL) has important regulatory functions in the host immune response. We studied antiinflammatory effects of endogenous and recombinant TRAIL (rTRAIL) in experimental meningitis. Following intrathecal application of pneumococcal cell wall, a TLR2 ligand, we found prolonged inflammation, augmented clinical impairment, and increased apoptosis in the hippocampus of TRAIL(-/-) mice. Administration of rTRAIL into the subarachnoid space of TRAIL(-/-) mice or reconstitution of hematopoiesis with wild-type bone marrow cells reversed these effects, suggesting an autoregulatory role of TRAIL within the infiltrating leukocyte population. Importantly, intrathecal application of rTRAIL in wild-type mice with meningitis also decreased inflammation and apoptosis. Moreover, patients suffering from bacterial meningitis showed increased intrathecal synthesis of TRAIL. Our findings provide what we believe is the first evidence that TRAIL may act as a negative regulator of acute CNS inflammation. The ability of TRAIL to modify inflammatory responses and to reduce neuronal cell death in meningitis suggests that it may be used as a novel antiinflammatory agent in invasive infections.

Indexed as

AnimalsCD18 AntigensCell SurvivalCytokinesDisease Models, AnimalGene Expression RegulationGenotypeGram-Positive CocciGranulocytesHippocampusHumansLeukocytesMaleMeningitis, BacterialMiceMice, Inbred C57BLCD18 AntigensCytokinesReceptors, TNF-Related Apoptosis-Inducing LigandRecombinant ProteinsTNF-Related Apoptosis-Inducing Ligand

Identifiers

PMID17571163
PMCPMC1888568
OpenAlexW2065218073

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.