Evidence map›Paper›PMID 29801457›Full record

ArticleJournal of translational medicine2018

Acquired immunological imbalance after surgery with cardiopulmonary bypass due to epigenetic over-activation of PU.1/M-CSF.

Krzysztof Laudanski, Mateusz Zawadka, Jacek Polosak, Jaymin Modi, Matthew DiMeglio, Jacob Gutsche, Wilson Y Szeto, Monika Puzianowska-Kuznicka

Abstract read
In one paragraph

Article in Journal of translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

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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

8 authors.

Krzysztof LaudanskiDepartment of Anesthesiology, University of Pennsylvania, Philadelphia, PA, 19146, USA. krzysztof.laudanski@uphs.upenn.edu.ORCID 0000-0002-7373-0851
Mateusz ZawadkaDepartment of Anesthesiology, Medical University of Warsaw, Warsaw, 02-091, Poland.
Jacek PolosakDepartment of Human Epigenetics, Mossakowski Medical Research Centre, Warsaw, 02-106, Poland.
Jaymin ModiPhiladelphia College of Osteopathic Medicine, Philadelphia, PA, 19131, USA.
Matthew DiMeglioPhiladelphia College of Osteopathic Medicine, Philadelphia, PA, 19131, USA.
Jacob GutscheDepartment of Anesthesiology, University of Pennsylvania, Philadelphia, PA, 19146, USA.
Wilson Y SzetoDivision of Cardiovascular Surgery, University of Pennsylvania, Philadelphia, PA, 19146, USA.
Monika Puzianowska-KuznickaDepartment of Human Epigenetics, Mossakowski Medical Research Centre, Warsaw, 02-106, Poland.

Funding

Epigenetic mediated long-term aberrations in myeloid cells after critical illnessK23GM120630 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI LAUDANSKI, KRZYSZTOF · 2017 to 2020
$783k
National Institute of General Medical Sciences (US) 1K23GM120630NIGMS NIH HHS K23 GM120630
6 · The paper itself

Abstract

backgroundIt has been shown that severe insult to the immune system may trigger prolonged macrophage characteristics associated with excessive release of monocyte colony stimulating factor (M-CSF). However, it is unclear how persistent is the macrophage-like characteristics in circulating monocytes (MO). In this study, 20 patients who underwent non-emergent cardiopulmonary bypass had their monocytes characterized before surgery and 3 months after surgery.

methodsWe assessed the macrophage characteristics of MO using cytokine production, surface marker expression, an ability to stimulate T cells, and methylation of the promoter region of the gene encoding PU.1, a critical component to M-CSF production. MO function as well as activation and differentiation potential were longitudinally assessed.

resultsAt 3 months after cardiopulmonary bypass, monocytes exhibited increased expression of MRP8, transforming growth factor-β/latency-associated peptide, suppressor of cytokine signaling 3 while phagocytic properties were increased. Concomitantly, we observed a decreased expression of CD86, a decreased ability to form regulatory dendritic cells, and a diminished ability to stimulate T cells. These characteristics were accompanied by a persistent increase in the secretion of M-CSF, over-activation of PU.1, and decreased methylation of the PU.1 promoter region. Serum levels of C-reactive protein and anti-cytomegalovirus IgG antibody titers were also elevated in some patients at 3 months after surgery.

conclusionsWe concluded that at 3 months after cardiopulmonary bypass, monocytes continued to express a new macrophage-like milieu that was associated with the persistent activation of the PU.1/M-CSF pathway.

Indexed as

Cardiopulmonary BypassEpigenesis, GeneticAgedBiomarkersFemaleHumansImmune SystemInflammation MediatorsMacrophage Colony-Stimulating FactorMaleMonocytesPhenotypePromoter Regions, GeneticProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Receptor, Macrophage Colony-Stimulating FactorBiomarkersInflammation MediatorsMacrophage Colony-Stimulating FactorProto-Oncogene ProteinsProto-Oncogene Protein Spi-1Receptor, Macrophage Colony-Stimulating FactorTrans-ActivatorsCardiopulmonary bypassEpigeneticsGranulocyte colony stimulating factorMonocytesPU.1

Identifiers

PMID29801457
PMCPMC5970449

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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.