Evidence map›Paper›PMID 9916064›Full record

ArticleInfection and immunity1999

Tumor necrosis factor alpha receptor I is important for survival from Streptococcus pneumoniae infections.

D P O'Brien, D E Briles, A J Szalai, A H Tu, I Sanz, M H Nahm

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
1.1field-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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 93 citations in OpenAlex.

  1. Pooled it
  2. Serum Tumor Necrosis Factor-Canadian respiratory journal · 2018
    Pooled it
  3. Pretransplant natural antibody levels identify a subset of deceased donor kidney transplant recipients that benefit from infliximab induction.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2025
    Trial
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  18. Pneumococci: immunology of the innate host response.Respirology (Carlton, Vic.) · 2010
    Review
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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

6 authors at 2 institutions in 1 country.

D P O'BrienDepartments of Pediatrics, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA.
D E Briles
A J Szalai
A H Tu
I Sanz
M H Nahm
University of Alabama at Birmingham · USPediatrics and Genetics · US

Funding

Impact of a new group 6 serotype on pneumococcal vaccinesR01AI031473 · NIAID · WASHINGTON UNIVERSITY · PI NAHM, MOON H. · 1991 to 2011
$1.7M
EVALUATION OF INFECTIOUS CONTROL MEASURES-266945248N01AI045248 · NIAID · UNIVERSITY OF ROCHESTER · 1994 to 2004
$500k
Pneumococcal capsule and host innate immunityR56AI031473 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI NAHM, MOON H. · 2012 to 2012
$366k
NIAID NIH HHS AI-31473NIAID NIH HHS N01 AI045248NIAID NIH HHS N01 AI-45248NIAID NIH HHS R01 AI031473NIAID NIH HHS R56 AI031473
6 · The paper itself

Abstract

Tumor necrosis factor alpha (TNF-alpha) is important in resistance to various microorganisms and provides signals to the target cells through two different receptors, TNF-alpha receptor I (TNFRI) (p55 receptor) and TNFRII (p75 receptor). To delineate the significance of the two different signaling pathways in resisting infections with extracellular bacteria, we examined the resistance of mice to Streptococcus pneumoniae (serotype 6B). TNF-alpha needs to be present early in infections, since one injection of wild-type mice with anti-TNF-alpha leads to an increased susceptibility of these mice to S. pneumoniae. TNF-alpha signaling through the p55 receptor (but not the p75 receptor) is crucial in resisting S. pneumoniae infections, because intraperitoneal injection of 100 CFU/mouse killed p55-deficient mice by day 2 of infection, whereas 1,000,000 CFU/mouse was needed to kill half of the control mice. p55-deficient mice do not show evidence of a deficient acute-phase response. All three types of mice (p55 deficient, p75 deficient, and normal) showed comparable rises in the levels of two acute-phase proteins (serum amyloid P and C3) at 24, 48, and 72 h after the experimental infections, and all of the mice showed comparable influxes of neutrophils to the site of infection. Finally, it was demonstrated that p55-deficient mice can be protected from the lethal effects of S. pneumoniae infection by injection of antibodies specific for S. pneumoniae polysaccharide capsule.

Indexed as

Acute-Phase ReactionAnimalsAntibodies, BacterialAntigens, CDDisease Models, AnimalDisease SusceptibilityGranulocytesLeukocyte CountMiceMice, Inbred C57BLNeutralization TestsPeritoneumPneumococcal InfectionsReceptors, Tumor Necrosis FactorReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IIAntibodies, BacterialAntigens, CDReceptors, Tumor Necrosis FactorReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IITumor Necrosis Factor-alpha

Identifiers

PMID9916064
PMCPMC96360
OpenAlexW2156015866

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.