Evidence map›Paper›PMID 19139724›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2009

Brain damage in newborn rat model of meningitis by Enterobacter sakazakii: a role for outer membrane protein A.

Rahul Mittal, Ying Wang, Catherine J Hunter, Ignacio Gonzalez-Gomez, Nemani V Prasadarao

Open access · bronzeAbstract read
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 86 citations in OpenAlex.

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  7. Frontiers in immunology · 2022
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  10. The Roles of Two Type VI Secretion Systems inFrontiers in microbiology · 2018
    Article
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  15. Article
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  17. Review
  18. Article
  19. Article
  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

5 authors at 1 institution in 1 country.

Rahul MittalDepartment of Pediatrics, Division of Infectious Diseases, The Saban Research Institute, Childrens Hospital Los Angeles, Los Angeles, CA 90027, USA.
Ying Wang
Catherine J Hunter
Ignacio Gonzalez-Gomez
Nemani V Prasadarao
Children's Hospital of Los Angeles · US

Funding

Brain Endothelial Receptor for E. coliR01AI040567 · NIAID · CHILDREN'S HOSPITAL OF LOS ANGELES · PI DAVIS, MARK E, GODDARD, WILLIAM ANDREW · 2001 to 2015
$5.5M
Maneuvering of Macrophage Function By Escherichia coli K1R01NS073115 · NINDS · CHILDREN'S HOSPITAL OF LOS ANGELES · PI NEMANI, PRASADARAO V · 2010 to 2014
$1.6M
BRAIN ENDOTHELIAL GLYCOPROTEIN INTERACTIVE WITH E COLIR29AI040567 · NIAID · CHILDREN'S HOSPITAL LOS ANGELES · PI NEMANI, PRASADARAO V · 1997 to 2001
$211k
NIAID NIH HHS AI40567NIAID NIH HHS R01 AI040567NIAID NIH HHS R29 AI040567NINDS NIH HHS R01 NS073115
6 · The paper itself

Abstract

Enterobacter sakazakii (ES) is an emerging pathogen that causes sepsis, meningitis, and necrotizing enterocolitis in neonates. Very limited information is available regarding the pathogenesis of these diseases and the specific virulence factors of ES. Here, we demonstrate, for the first time using a newborn rat model, that outer membrane protein A (OmpA) expression is important for the onset of meningitis by ES. Orally administered OmpA(+) ES traverses the intestinal barrier, multiplies in blood, and subsequently penetrates the blood-brain barrier. OmpA(+) ES were present in high numbers in the brains of infected animals along with associated neutrophil infiltration, hemorrhage, and gliosis. In contrast, OmpA(-) ES could not bind to the intestinal epithelial cells in vitro and in vivo efficiently. The bound OmpA(+) ES also caused apoptosis of enterocytes in the intestinal segments of infected animals; OmpA(-) ES did not. Furthermore, OmpA(-) ES are very susceptible to blood and serum killing, whereas OmpA(+) ES are resistant. Of note, 100% mortality rates were observed in OmpA(+) ES-infected newborn rats, whereas OmpA(-) ES-infected rats survived without any pathological manifestations. The inability of OmpA(-) ES to cause disease was restored by complementation with the ompA gene. These results suggest that OmpA expression in ES is necessary for the colonization of the gastrointestinal tract and for subsequent survival in blood to cause meningitis.

Indexed as

AnimalsAnimals, NewbornApoptosisBacterial Outer Membrane ProteinsBloodBlood Bactericidal ActivityBrainCronobacter sakazakiiCytokinesDisease Models, AnimalEnterobacteriaceae InfectionsEnterocytesGliosisImmunohistochemistryIntestinal MucosaIntracranial HemorrhagesBacterial Outer Membrane ProteinsCytokinesOMPA outer membrane proteins

Identifiers

PMID19139724
PMCPMC3256236
OpenAlexW1979209211

What OpenQuestion holds

Textmetadata
LicenceTDM
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.