Evidence map›Paper›PMID 23860351›Full record

ReviewToxins2013

Mini-review: novel therapeutic strategies to blunt actions of pneumolysin in the lungs.

Rudolf Lucas, Istvan Czikora, Supriya Sridhar, Evgeny Zemskov, Boris Gorshkov, Umapathy Siddaramappa, Aluya Oseghale, Jonathan Lawson, Alexander Verin, Ferenc G Rick and 6 more

Open access · goldAbstract readReview
In one paragraph

Review in Toxins, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Review
  6. The Epithelial Sodium Channel-An Underestimated Drug Target.International journal of molecular sciences · 2023
    Review
  7. Review
  8. Review
  9. Article
  10. Toxins · 2021
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. 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

16 authors at 3 institutions in 2 countries.

Rudolf LucasVascular Biology Center, Georgia Regents University, Augusta, GA 30912, USA. rlucas@gru.edu
Istvan Czikora
Supriya Sridhar
Evgeny Zemskov
Boris Gorshkov
Umapathy Siddaramappa
Aluya Oseghale
Jonathan Lawson
Alexander Verin
Ferenc G Rick
Norman L Block
Helena Pillich
Maritza Romero
Martin Leustik
Andrew V Schally
Trinad Chakraborty
Augusta University · USJustus-Liebig-Universität Gießen · DEUniversity of Miami · US

Funding

Protective activity of the lectin-like domain of TNF in permeability edemaR01HL094609 · NHLBI · AUGUSTA UNIVERSITY · PI LUCAS, RUDOLF · 2010 to 2013
$1.5M
NHLBI NIH HHS R01 HL094609NHLBI NIH HHS R01HL094609
6 · The paper itself

Abstract

Severe pneumonia is the main single cause of death worldwide in children under five years of age. The main etiological agent of pneumonia is the G+ bacterium Streptococcus pneumoniae, which accounts for up to 45% of all cases. Intriguingly, patients can still die days after commencing antibiotic treatment due to the development of permeability edema, although the pathogen was successfully cleared from their lungs. This condition is characterized by a dramatically impaired alveolar epithelial-capillary barrier function and a dysfunction of the sodium transporters required for edema reabsorption, including the apically expressed epithelial sodium channel (ENaC) and the basolaterally expressed sodium potassium pump (Na+-K+-ATPase). The main agent inducing this edema formation is the virulence factor pneumolysin, a cholesterol-binding pore-forming toxin, released in the alveolar compartment of the lungs when pneumococci are being lysed by antibiotic treatment or upon autolysis. Sub-lytic concentrations of pneumolysin can cause endothelial barrier dysfunction and can impair ENaC-mediated sodium uptake in type II alveolar epithelial cells. These events significantly contribute to the formation of permeability edema, for which currently no standard therapy is available. This review focuses on discussing some recent developments in the search for the novel therapeutic agents able to improve lung function despite the presence of pore-forming toxins. Such treatments could reduce the potentially lethal complications occurring after antibiotic treatment of patients with severe pneumonia.

Indexed as

AnimalsBacterial ProteinsChild, PreschoolDisease Models, AnimalGrowth HormoneHumansImmune SystemLectinsLungPneumoniaPulmonary EdemaStreptococcus pneumoniaeStreptolysinsStructure-Activity RelationshipTumor Necrosis Factor-alphaVirulence FactorsBacterial ProteinsGrowth HormoneLectinsplY protein, Streptococcus pneumoniaeStreptolysinsTumor Necrosis Factor-alphaVirulence Factors

Identifiers

PMID23860351
PMCPMC3737495
OpenAlexW2040000151

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.