Evidence map›Paper›PMID 30896813›Full record

ArticleMolecular medicine reports2019

Targeting bacterial quorum sensing shows promise in improving intestinal barrier function following burn‑site infection.

Fatemeh Adiliaghdam, Marianna Almpani, Mohammad Hadi Gharedaghi, Mehran Najibi, Richard A Hodin, Laurence G Rahme

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

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  12. Antibiotics (Basel, Switzerland) · 2020
    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

6 authors at 2 institutions in 1 country.

Fatemeh AdiliaghdamDepartment of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Marianna AlmpaniDepartment of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Mohammad Hadi GharedaghiDepartment of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Mehran NajibiDepartment of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Richard A HodinDepartment of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Laurence G RahmeDepartment of Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
Massachusetts General Hospital · USHarvard University · US

Funding

Interruption of Signaling-Mediated Bacterial Persistent InfectionsR33AI105902 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI RAHME, LAURENCE G · 2015 to 2017
$1.8M
NIAID NIH HHS R33 AI105902
6 · The paper itself

Abstract

Burn‑site infections, commonly due to Pseudomonas aeruginosa, have been associated with deranged intestinal integrity, allowing bacteria and their products to translocate from the gut to the circulatory system. The P. aeruginosa quorum sensing (QS) transcription factor MvfR (PqsR) controls the expression of numerous virulence factors, and the synthesis of several toxic products. However, the role of QS in intestinal integrity alterations, to the best of our knowledge, has not been previously investigated. Using a proven anti‑MvfR, anti‑virulence agent, the in vivo results of the present study revealed that inhibition of MvfR function significantly decreased Fluorescein Isothiocyanate‑Dextran (FITC‑Dextran) flow from the intestine to the systemic circulation, diminished bacterial translocation from the intestine to mesenteric lymph nodes (MLNs), and improved tight junction integrity in thermally injured and infected mice. In addition, the MvfR antagonist administration alleviates the intestinal inflammation, as demonstrated by reduced ileal TNF‑α and fecal lipocalin‑2 concentrations. In addition, it is associated with lower levels of circulating endotoxin and decreased P. aeruginosa dissemination from the burn wound to the ileum. Collectively, these results hold great promise that the inhibition of this QS system mitigates gut hyperpermeability by attenuating the derangement of morphological and immune aspects of the intestinal barrier, suggesting that MvfR function is crucial in the deterioration of intestinal integrity following P. aeruginosa burn‑site infection. Therefore, an anti‑virulence approach targeting MvfR, could potentially offer a novel therapeutic approach against multi‑drug resistant P. aeruginosa infections following thermal injuries. Since this approach is targeting virulence pathways that are non‑essential for growth or viability, our strategy is hypothesized to minimize the development of bacterial resistance, and preserve the beneficial enteric microbes, while improving intestinal integrity that is deranged as a result of burn and infection.

Indexed as

Quorum SensingAnimalsAnti-Bacterial AgentsBacterial ProteinsBurnsDrug Resistance, BacterialEndotoxinsIntestinal MucosaMaleMiceMice, Inbred C57BLPseudomonas aeruginosaPseudomonas InfectionsTranscription FactorsTumor Necrosis Factor-alphaVirulenceAnti-Bacterial AgentsBacterial ProteinsEndotoxinsTranscription FactorsTumor Necrosis Factor-alpha

Identifiers

PMID30896813
PMCPMC6472113
OpenAlexW2924170030

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.