Evidence map›Paper›PMID 18694970›Full record

ArticleInfection and immunity2008

Mouse model of hemolytic-uremic syndrome caused by endotoxin-free Shiga toxin 2 (Stx2) and protection from lethal outcome by anti-Stx2 antibody.

Kristin A D Sauter, Angela R Melton-Celsa, Kay Larkin, Megan L Troxell, Alison D O'Brien, Bruce E Magun

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.8field-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

43 citing papers in PubMed, 76 citations in OpenAlex.

  1. Article
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  5. Targeting the innate repair receptor axisFrontiers in immunology · 2022
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  16. Baicalin inhibits the lethality of Shiga-like toxin 2 in mice.Antimicrobial agents and chemotherapy · 2015
    Article
  17. Article
  18. Article
  19. Article
  20. Review
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.

Kristin A D SauterDepartment of Cell and Developmental Biology, Oregon Health and Science University, Portland, Oregon 97239, USA.
Angela R Melton-Celsa
Kay Larkin
Megan L Troxell
Alison D O'Brien
Bruce E Magun
Oregon Health & Science University · USUniformed Services University of the Health Sciences · US

Funding

Pathogenicity of Shiga Toxin Producing E.coliR37AI020148 · NIAID · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI O'BRIEN, ALISON DAVIS · 2008 to 2016
$3.8M
SHIGA-LIKE TOXIN OF ESCHERICHIA COLIR01AI020148 · NIAID · U.S. UNIFORMED SERVICES UNIV OF HLTH SCI · PI MELTON-CELSA, ANGELA · 1987 to 2017
$3.3M
Proinflammatory signaling in the kidney by Shiga toxinF31DK079419 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI SAUTER, KRISTIN AD · 2007 to 2009
$121k
SHIGA-LIKE TOXIN OF ESCHERICHIA COLIR22AI020148 · NIAID · U.S. UNIFORMED SERVICES UNIV OF HLTH SCI · PI O'BRIEN, ALISON DAVIS · 1985 to 1991
–
NIAID NIH HHS AI1059335NIAID NIH HHS AI20148NIAID NIH HHS R01 AI020148NIAID NIH HHS R37 AI020148NIDDK NIH HHS DK079419NIDDK NIH HHS F31 DK079419NIEHS NIH HHS ES889456
6 · The paper itself

Abstract

Hemolytic-uremic syndrome (HUS) results from infection by Shiga toxin (Stx)-producing Escherichia coli and is the most common cause of acute renal failure in children. We have developed a mouse model of HUS by administering endotoxin-free Stx2 in multiple doses over 7 to 8 days. At sacrifice, moribund animals demonstrated signs of HUS: increased blood urea nitrogen and serum creatinine levels, proteinuria, deposition of fibrin(ogen), glomerular endothelial damage, hemolysis, leukocytopenia, and neutrophilia. Increased expression of proinflammatory chemokines and cytokines in the sera of Stx2-treated mice indicated a systemic inflammatory response. Currently, specific therapeutics for HUS are lacking, and therapy for patients is primarily supportive. Mice that received 11E10, a monoclonal anti-Stx2 antibody, 4 days after starting injections of Stx2 recovered fully, displaying normal renal function and normal levels of neutrophils and lymphocytes. In addition, these mice showed decreased fibrin(ogen) deposition and expression of proinflammatory mediators compared to those of Stx2-treated mice in the absence of antibody. These results indicate that, when performed during progression of HUS, passive immunization of mice with anti-Stx2 antibody prevented the lethal effects of Stx2.

Indexed as

AnimalsAntibodies, BacterialAntibodies, MonoclonalAntitoxinsBlood Urea NitrogenChildCreatinineCytokinesFibrinogenHemolytic-Uremic SyndromeHumansImmunohistochemistryKidneyLeukopeniaMiceMice, Inbred C57BLAntibodies, BacterialAntibodies, MonoclonalAntitoxinsCreatinineCytokinesFibrinogenShiga Toxin 2

Identifiers

PMID18694970
PMCPMC2546846
OpenAlexW2120566226

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.