Evidence map›Paper›PMID 36347039›Full record

ArticleInternational journal of immunopathology and pharmacology

PM2.5 activated NLRP3 inflammasome and IL-1β release in MH-S cells by facilitating autophagy via activating Wnt5a.

Guanli Yuan, Yinfeng Liu, Zheng Wang, Xiaotong Wang, Zhuoxiao Han, Xixin Yan, Aihong Meng

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of immunopathology and pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.3field-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

6 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. The therapeutic potential of RNA m(6)A in lung cancer.Cell communication and signaling : CCS · 2024
    Review
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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 2 institutions in 1 country.

Guanli YuanDepartment of Respiratory and Critical Care Medicine, 71213The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Yinfeng LiuDepartment of Breast Surgery, 561060The First Hospital of Qinhuangdao, Qinhuangdao, China.
Zheng WangDepartment of Respiratory and Critical Care Medicine, 71213The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Xiaotong WangDepartment of Respiratory and Critical Care Medicine, 71213The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Zhuoxiao HanDepartment of Breast Surgery, 561060The First Hospital of Qinhuangdao, Qinhuangdao, China.
Xixin YanDepartment of Respiratory and Critical Care Medicine, 71213The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Aihong MengDepartment of Respiratory and Critical Care Medicine, 71213The Second Hospital of Hebei Medical University, Shijiazhuang, China.ORCID 0000-0003-4340-2424
Hebei Medical University · CNFirst Hospital of Qinhuangdao · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Particulate matter 2.5 (PM2.5)-induced pulmonary inflammation is an important issue worldwide. NLRP3 inflammasome activation has been found to be involved in pulmonary inflammation development. However, whether PM2.5 induces pulmonary inflammation by activating the NLRP3 inflammasome has not yet been fully elucidated. This study researched whether PM2.5 induces the NLRP3 inflammasomes activation to trigger pulmonary inflammation.Mice and MH-S cells were exposed to PM2.5, BOX5, and Rapamycin. Hematoxylin and eosin staining was performed on the lung tissues of mice. M1 macrophage marker CD80 expression in the lung tissues of mice and LC3B expression in MH-S cells was detected by immunofluorescence. IL-1β level in the lavage fluid and MH-S cells were detected by enzyme-linked immunosorbent assay. Protein expression was detected by Western blot. Autophagy assay in MH-S cells was performed by LC3B-GFP punctae experiment.PM2.5 exposure induced the lung injury of mice and increased NLRP3, P62, Wnt5a, LC3BII/I, and CD80 expression and IL-1β release in the lung tissues. PM2.5 treatment increased NLRP3, pro-caspase-1, cleaved caspase-1, Pro-IL-1β, Pro-IL-18, P62, LC3BII/I, and Wnt5a expression, IL-1β release, and LC3B-GFP punctae in MH-S cells. However, BOX5 treatment counteracted this effect of PM2.5 on lung tissues of mice and MH-S cells. Rapamycin reversed the effect of BOX5 on PM2.5-induced lung tissues of mice and MH-S cells.PM2.5 activated the NLRP3 inflammasome and IL-1β release in MH-S cells by facilitating the autophagy via activating Wnt5a. The findings of this study provided a new clue for the treatment of pulmonary inflammation caused by PM2.5.

Indexed as

InflammasomesPneumoniaAutophagyCaspase 1HumansInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinParticulate MatterSirolimusWnt-5a ProteinCaspase 1InflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinParticulate MatterSirolimusWnt-5a ProteinWNT5A protein, humanautophagyIL-1β releaseNLRP3 inflammasomePM2.5pulmonary inflammationWnt5a

Identifiers

PMID36347039
PMCPMC9647284
OpenAlexW4308687091

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.