Evidence map›Paper›PMID 20413631›Full record

ArticleAmerican journal of respiratory and critical care medicine2010

Insulin-like growth factor-1 levels contribute to the development of bacterial translocation in sepsis.

Gary W Hunninghake, Kevin C Doerschug, Amanda B Nymon, Gregory A Schmidt, David K Meyerholz, Alix Ashare

Abstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 58 citations in OpenAlex.

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  17. Bacterial Dissemination to the Brain in Sepsis.American journal of respiratory and critical care medicine · 2018
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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 2 countries.

Gary W HunninghakeDepartment of Internal Medicine, University of Iowa Roy J. and Lucille A. Carver College of Medicine, Iowa City, Iowa, USA.
Kevin C Doerschug
Amanda B Nymon
Gregory A Schmidt
David K Meyerholz
Alix Ashare
Institute of Occupational Medicine · SGUniversity of Iowa · US

Funding

UNIVERSITY OF IOWA CTSA FOR PEDIATRIC RESEARCHUL1RR024979 · NCRR · UNIVERSITY OF IOWA · PI ROSENTHAL, GARY E · 2007 to 2011
$31.8M
Role of PI3K in Sepsis-induced Acute Lung InjuryR01HL073967 · NHLBI · UNIVERSITY OF IOWA · PI HUNNINGHAKE, GARY W · 2003 to 2006
$1.5M
Modulation of Acute Lung InjuryR01HL077431 · NHLBI · UNIVERSITY OF IOWA · PI HUNNINGHAKE, GARY W · 2004 to 2007
$1.4M
Liver Injury/Sepsis-Induced Multiple Organ Dysfunction SK08DK073519 · NIDDK · UNIVERSITY OF IOWA · PI ASHARE, ALIX · 2006 to 2010
$656k
The Organ Specific Role of Superoxide Dismutase in SepsisR03DK084057 · NIDDK · DARTMOUTH COLLEGE · PI ASHARE, ALIX · 2009 to 2010
$157k
NCRR NIH HHS UL1 RR024979NCRR NIH HHS UL1RR024979NHLBI NIH HHS HL-073967-02NHLBI NIH HHS HL-077431-01NIAID NIH HHS L30 AI062287NIDDK NIH HHS K08DK073519NIDDK NIH HHS R03 DK084057
6 · The paper itself

Abstract

rationaleMany lines of evidence point toward the gastrointestinal (GI) tract in the pathophysiology of organ dysfunction in sepsis. Splanchnic hypoperfusion during sepsis leads to enterocyte apoptosis, diminished barrier function, and release of bacterial products. Sepsis lowers levels of insulin-like growth factor (IGF)-1, a known antiapoptotic factor. We recently demonstrated that treatment with IGF-1 is protective in murine sepsis.

objectivesWe hypothesize that decreased IGF-1 levels in sepsis contributes to the development of bacterial translocation.

methodsSepsis was induced in C57BL/6 mice via intratracheal instillation of Pseudomonas aeruginosa. Human subjects with sepsis were enrolled if they had a documented positive blood culture with a nonenteric organism. Bacterial translocation was measured in serum by quantitative real-time polymerase chain reaction with primers specific for enteric bacteria. Serum IGF-1 was measured by ELISA. Apoptosis of the GI epithelium was assessed via immunohistochemistry. MEASUREMENTS AND MAIN

resultsWe found that mice with severe sepsis had evidence of bacterial translocation by 24 hours. Enteric bacterial load correlated inversely with levels of serum IGF-1. If we treated mice with IGF-1, bacterial translocation was significantly decreased. In addition, we found increased GI epithelial cell apoptosis after sepsis, which was significantly decreased after IGF-1 treatment. Human subjects with nonenteric sepsis developed progressive enteric bacteremia over 3 days. The degree of enteric bacteremia correlated inversely with serum IGF-1 levels.

conclusionsThese data support the hypothesis that sepsis-induced reductions in IGF-1 levels contribute to the development of bacterial translocation in both a murine model and human subjects.

Indexed as

Bacterial TranslocationAnalysis of VarianceAnimalsApoptosisDisease Models, AnimalEnterocytesEnzyme-Linked Immunosorbent AssayFemaleHumansInsulin-Like Growth Factor IIntestinal MucosaMaleMiceMice, Inbred C57BLMiddle AgedPseudomonas aeruginosaInsulin-Like Growth Factor I

Identifiers

PMID20413631
PMCPMC2937242
OpenAlexW2107989776

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.