Evidence map›Paper›PMID 32248343›Full record

ArticleImmunologic research2020

TLR-2-mediated metabolic reprogramming participates in polyene phosphatidylcholine-mediated inhibition of M1 macrophage polarization.

Ting-Ting Feng, Xiao-Ying Yang, Shan-Shan Hao, Fen-Fen Sun, Ye Huang, Qi-Si Lin, Wei Pan

Abstract read
PubMed Publisher
In one paragraph

Article in Immunologic research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 28 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Ting-Ting FengJiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Xuzhou Medical University, Tongshan Road 209, Xuzhou, 221004, Jiangsu Province, People's Republic of China.
Xiao-Ying YangJiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Medical University, Tongshan Road 209, Xuzhou, 221004, Jiangsu Province, People's Republic of China.
Shan-Shan HaoJiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Medical University, Tongshan Road 209, Xuzhou, 221004, Jiangsu Province, People's Republic of China.
Fen-Fen SunJiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Medical University, Tongshan Road 209, Xuzhou, 221004, Jiangsu Province, People's Republic of China.
Ye HuangJiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Xuzhou Medical University, Tongshan Road 209, Xuzhou, 221004, Jiangsu Province, People's Republic of China.
Qi-Si LinJiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Xuzhou Medical University, Tongshan Road 209, Xuzhou, 221004, Jiangsu Province, People's Republic of China. qslin074@126.com.
Wei PanJiangsu Key Laboratory of Immunity and Metabolism, Department of Pathogenic Biology and Immunology, Xuzhou Medical University, Tongshan Road 209, Xuzhou, 221004, Jiangsu Province, People's Republic of China. panwei525@126.com.
Xuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study aimed to investigate whether the classic hepatoprotective drug polyene phosphatidylcholine (PPC) regulates macrophage polarization and explores the potential role of TLR-2 in this process. In RAW264.7 macrophages and murine bone marrow-derived macrophages (BMDMs) stimulated by lipopolysaccharide (LPS), PPC significantly inhibited the production of IL-6, TNF-α, and the mRNA expression of M1-type macrophage markers. Consistently, PPC reduced the mRNA expression of several key enzymes in the pathways of glycolysis and lipid synthesis while increasing the expression of key enzymes associated with lipid oxidation. Moreover, blocking the glycolytic pathway using 2-deoxy-D-glucose (2-DG) significantly enhanced the anti-inflammatory effect of PPC. However, inhibition of lipid oxidation using GW9662 (an inhibitor of PPAR-γ) and GW6471 (an inhibitor of PPAR-α) abolished the anti-inflammatory effect of PPC. Interestingly, TLR-2 expression in macrophages was significantly downregulated after exposure to PPC. Moreover, pre-activation of TLR-2 hampered the anti-inflammatory effect of PPC. In addition, PPC did not inhibit the secretion of IL-6 and TNF-α in TLR-2

Indexed as

AnimalsAnti-Inflammatory AgentsCell DifferentiationCellular ReprogrammingFemaleInterleukin-6Lipid PeroxidationLipopolysaccharidesMacrophagesMiceMice, Inbred C57BLMice, KnockoutPhosphatidylcholinesRAW 264.7 CellsSignal TransductionTh1 CellsAnti-Inflammatory AgentsInterleukin-6LipopolysaccharidesPhosphatidylcholinesTlr2 protein, mouseToll-Like Receptor 2Tumor Necrosis Factor-alphaMacrophage polarizationMetabolic reprogrammingPolyene phosphatidylcholineTLR-2

Identifiers

PMID32248343
OpenAlexW3014987953

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.