Evidence map›Paper›PMID 34733114›Full record

ArticleMediators of inflammation2021

Increased Death of Peripheral Blood Mononuclear Cells after TLR4 Inhibition in Sepsis Is Not via TNF/TNF Receptor-Mediated Apoptotic Pathway.

Chien-Ming Chu, Li-Chung Chiu, Chung-Chieh Yu, Li-Pang Chuang, Kuo-Chin Kao, Li-Fu Li, Huang-Pin Wu

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Electroacupuncture at ST36 (Journal of inflammation research · 2022
    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

7 authors at 2 institutions in 1 country.

Chien-Ming ChuDivision of Pulmonary, Critical Care and Sleep Medicine, Chang Gung Memorial Hospital, Keelung 204, Taiwan.
Li-Chung ChiuDepartment of Pulmonary and Critical Care Medicine, Chang Gung Memorial Hospital, Taoyuan 333, Taiwan and.
Chung-Chieh YuDivision of Pulmonary, Critical Care and Sleep Medicine, Chang Gung Memorial Hospital, Keelung 204, Taiwan.
Li-Pang ChuangDepartment of Pulmonary and Critical Care Medicine, Chang Gung Memorial Hospital, Taoyuan 333, Taiwan and.
Kuo-Chin KaoDepartment of Pulmonary and Critical Care Medicine, Chang Gung Memorial Hospital, Taoyuan 333, Taiwan and.
Li-Fu LiDivision of Pulmonary, Critical Care and Sleep Medicine, Chang Gung Memorial Hospital, Keelung 204, Taiwan.
Huang-Pin WuDivision of Pulmonary, Critical Care and Sleep Medicine, Chang Gung Memorial Hospital, Keelung 204, Taiwan.ORCID https://orcid.org/0000-0002-8906-4566
Chang Gung University · TWChang Gung Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundApoptosis is one of the causes of immune depression in sepsis. Pyroptosis also occurs in sepsis. The toll-like receptor (TLR) 4 and receptor for advanced glycation end products (RAGE) have been shown to play important roles in apoptosis and pyroptosis. However, it is still unknown whether TLR4 inhibition decreases apoptosis in sepsis.

methodsStimulated peripheral blood mononuclear cells (PBMCs) with or without lipopolysaccharides (LPS) and high-mobility group box 1 (HMGB1) were cultured with or without TLR4 inhibition using monoclonal antibodies from 20 patients with sepsis. Caspase-3, caspase-8, and caspase-9 activities were measured. The expression of B cell lymphoma 2 (Bcl2) and Bcl2-associated X (Bax) was measured. The cell death of PBMCs was detected using a flow cytofluorimeter.

resultsAfter TLR4 inhibition, Bcl2 to Bax ratio elevated both in LPS and HMGB1-stimulated PBMCs. The activities of caspase-3, caspase-8, and caspase-9 did not change in LPS or HMGB1-stimulated PBMCs. The cell death of LPS and HMGB1-stimulated CD8 lymphocytes and monocytes increased after TLR4 inhibition. The cell death of CD4 lymphocytes was unchanged.

conclusionThe apoptosis did not decrease, while TLR4 was inhibited. After TLR4 inhibition, there was an unknown mechanism to keep cell death in stimulated PBMCs in patients with sepsis.

Indexed as

AgedAntigens, NeoplasmApoptosisCaspasesCells, CulturedFemaleHMGB1 ProteinHumansLeukocytes, MononuclearLipopolysaccharidesMaleMitogen-Activated Protein KinasesPyroptosisReceptors, Tumor Necrosis FactorSepsisToll-Like Receptor 4Antigens, NeoplasmCaspasesHMGB1 ProteinLipopolysaccharidesMitogen-Activated Protein KinasesMOK protein, humanReceptors, Tumor Necrosis FactorToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID34733114
PMCPMC8560265
OpenAlexW3209238819

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.