Evidence map›Paper›PMID 26195547›Full record

ArticleInfection and immunity2015

Pseudomonas aeruginosa Quorum Sensing Molecule N-(3-Oxododecanoyl)-L-Homoserine-Lactone Induces HLA-G Expression in Human Immune Cells.

Daria Bortolotti, Joel LeMaoult, Claudio Trapella, Dario Di Luca, Edgardo D Carosella, Roberta Rizzo

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. HowInternational journal of molecular sciences · 2023
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Mechanisms and Targeted Therapies for Pseudomonas aeruginosa Lung Infection.American journal of respiratory and critical care medicine · 2018
    Review
  10. Review
  11. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Daria BortolottiDepartment of Medical Sciences, Section of Microbiology and Medical Genetics, University of Ferrara, Ferrara, Italy.
Joel LeMaoultCEA, Institute of Emerging Diseases and Innovative Therapies (iMETI), Research Division in Hematology and Immunology (SRHI), Saint-Louis Hospital, Paris, France.
Claudio TrapellaDepartment of Chemical and Pharmaceutical Sciences, University of Ferrara, Ferrara, Italy.
Dario Di LucaDepartment of Medical Sciences, Section of Microbiology and Medical Genetics, University of Ferrara, Ferrara, Italy.
Edgardo D CarosellaCEA, Institute of Emerging Diseases and Innovative Therapies (iMETI), Research Division in Hematology and Immunology (SRHI), Saint-Louis Hospital, Paris, France.
Roberta RizzoDepartment of Medical Sciences, Section of Microbiology and Medical Genetics, University of Ferrara, Ferrara, Italy rbr@unife.it.
University of Ferrara · ITCommissariat à l'Énergie Atomique et aux Énergies Alternatives · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HLA-G is a nonclassical class I human leukocyte antigen (HLA) involved in mechanisms of immune tolerance. The objective of this study was to determine whether N-(3-oxododecanoyl)-l-homoserine lactone (3O-C12-HSL), a quorum sensing molecule produced by Pseudomonas aeruginosa, could modify HLA-G expression to control the host immune response. We evaluated the ability of 3O-C12-HSL to induce HLA-G expression in primary immune cells, monocytes (U937 and THP1), and T-cell lines (Jurkat) in vitro and analyzed the cellular pathway responsible for HLA-G expression. We studied the HLA-G promoter with a luciferase assay and interleukin-10 (IL-10) and p38/CREB signaling with enzyme-linked immunosorbent assay and immunofluorescence, respectively. We observed that 3O-C12-HSL is able to induce HLA-G expression in human monocytes and T cells. We showed that the induction of HLA-G by 3O-C12-HSL is p38/CREB and IL-10 dependent. 3O-C12-HSL treatment is able to arrest only the U937 cell cycle, possibly due to the peculiar expression of the ILT2 receptor in the U937 cell line. Our observations suggest HLA-G as a mechanism to create a protected niche for the bacterial reservoir, similar to the role of HLA-G molecules during viral infections.

Indexed as

Quorum SensingUp-Regulation4-ButyrolactoneHLA-G AntigensHomoserineHumansInterleukin-10MonocytesPseudomonas aeruginosaPseudomonas InfectionsT-LymphocytesU937 Cells4-ButyrolactoneHLA-G AntigensHomoserineIL10 protein, humanInterleukin-10N-(3-oxododecanoyl)homoserine lactone

Identifiers

PMID26195547
PMCPMC4567644
OpenAlexW1596251670

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.