Evidence map›Paper›PMID 32504162›Full record

ArticleInflammation2020

PM2.5 Exposure Induces Inflammatory Response in Macrophages via the TLR4/COX-2/NF-κB Pathway.

Huiying Fu, Xia Liu, Wei Li, Yuyao Zu, Fangmei Zhou, Qiyang Shou, Zhishan Ding

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 2 pooled it
4.4field-weighted citation impact, top 4% 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

52 citing papers in PubMed, 2 syntheses or guidelines pooled it, 85 citations in OpenAlex.

  1. Pooled it
  2. The impact of particulate matter 2.5 on the risk of hepatocellular carcinoma: a meta-analysis.International archives of occupational and environmental health · 2022
    Pooled it
  3. Article
  4. Article
  5. Senolytics Reverse PMCardiovascular toxicology · 2026
    Article
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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.

Huiying Fu *The Second Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Xia Liu *The Second Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Wei LiCollege of Medical Technology, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Yuyao ZuCollege of Medical Technology, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Fangmei ZhouCollege of Medical Technology, Zhejiang Chinese Medical University, Hangzhou, 310053, China.
Qiyang ShouThe Second Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou, 310053, China. sqy133@126.com.
Zhishan DingCollege of Medical Technology, Zhejiang Chinese Medical University, Hangzhou, 310053, China. dzszjtcm@163.com.ORCID http://orcid.org/0000-0001-5740-1479
Zhejiang Chinese Medical University · CN

Funding

National Natural Science Foundation of China 81573677National Natural Science Foundation of China 81673645National Natural Science Foundation of China 81673672National Natural Science Foundation of China 81873047Natural Science Foundation of Zhejiang Province LQ17H030006
6 · The paper itself

Abstract

Fine particulate matter with an aerodynamic diameter less than 2.5 μm (PM2.5) is a serious air pollutant associated with health problems. Macrophages play an important role in the process of PM2.5-induced inflammation in respiratory diseases. However, the detailed mechanism remains unclear. We aimed to examine the mechanism of PM2.5-induced inflammation and find possible anti-inflammatory inhibitors. PM2.5 was collected in Hangzhou, China, and the composition of adsorbed materials on PM2.5 was characterized. RAW 254.7 cells were then treated with PM2.5. Phagocytosis was observed, and inflammatory response was triggered as demonstrated by the release of high levels of monocyte chemoattractant protein-1(MCP-1), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) and increased mRNA expression of inducible nitric oxide synthase (iNOS) and TNF-α. Treatment with classic inhibitors suppressed the released pro-inflammatory factors in a dose-dependent manner. Using Immunology Inflammation Compound Library, we screened 70 inhibitors and clustered them based on similarities in their inhibitory effects, which we detected using cytometric bead array (CBA) assay. Molecular analysis revealed that the expression of toll-like receptor 4 (TLR4), nuclear factor kappa-B (NF-κB), and cyclooxygenase-2 (COX-2) was increased in PM2.5-stimulated RAW 254.7 cells. Corresponding inhibitors were selected, and the CBA assay verified their anti-inflammatory effects. These inhibitors reduced the expression of pro-inflammatory factors, and this reduction was correlated with the downregulation of the TLR4/NF-κB/COX-2 signaling pathway. In conclusion, PM2.5 induces an inflammatory response in macrophages via activation of TLR4/NF-κB/COX-2 signaling, and the inhibitors of this pathway are potential therapeutic candidates to treat inflammatory disorders.

Indexed as

AnimalsCyclooxygenase 2Inflammation MediatorsMacrophagesMiceNF-kappa BParticulate MatterRAW 264.7 CellsSignal TransductionToll-Like Receptor 4Cyclooxygenase 2Inflammation MediatorsNF-kappa BParticulate MatterTlr4 protein, mouseToll-Like Receptor 4COX-2inflammationmacrophagesNF-κBPM2.5TLR4

Identifiers

PMID32504162
OpenAlexW3033910369

What Socratic 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 Socratic graph.