Combined transcriptome and microbiome analysis reveals the thyrotoxic effects of PM2.5 in female rats DOI Creative Commons
Xinwen Dong, Xiaofeng Han, Sanqiao Yao

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2024, Volume and Issue: 284, P. 116879 - 116879

Published: Aug. 13, 2024

Pervasive environmental pollutants, specifically particulate matter (PM

Language: Английский

The Effects and Pathogenesis of PM2.5 and Its Components on Chronic Obstructive Pulmonary Disease DOI Creative Commons
Qi Wang, Sha Liu

International Journal of COPD, Journal Year: 2023, Volume and Issue: Volume 18, P. 493 - 506

Published: April 1, 2023

Chronic obstructive pulmonary disease (COPD), a heterogeneous disease, is the leading cause of death worldwide. In recent years, air pollution, especially particulate matter (PM), has been widely studied as contributing factor to COPD. As an essential component PM, PM2.5 associated with COPD prevalence, morbidity, and acute exacerbations. However, specific pathogenic mechanisms were still unclear deserve further research. The diversity complexity components make it challenging get its accurate effects for It determined that most toxic are metals, polycyclic aromatic hydrocarbons (PAHs), carbonaceous particles (CPs), other organic compounds. PM2.5-induced cytokine release oxidative stress main reported Nonnegligibly, microorganism in PM 2.5 may directly mononuclear inflammation or break balance development exacerbation This review focuses on pathophysiology consequences

Language: Английский

Citations

62
Non-coding RNAs: An emerging player in particulate matter 2.5-mediated toxicity DOI
Seyed Mohsen Aghaei Zarch, Iraj Alipourfard, Hassan Rasoulzadeh

et al.

International Journal of Biological Macromolecules, Journal Year: 2023, Volume and Issue: 235, P. 123790 - 123790

Published: Feb. 22, 2023

Language: Английский

Citations

28
Nicotinamide phosphoribosyltransferase prompts bleomycin-induced pulmonary fibrosis by driving macrophage M2 polarization in mice DOI Creative Commons
Ya-Ling Chen, Tong Wang, Fuxiang Liang

et al.

Theranostics, Journal Year: 2024, Volume and Issue: 14(7), P. 2794 - 2815

Published: Jan. 1, 2024

Rationale: Idiopathic pulmonary fibrosis (IPF) is an irreversible, fatal interstitial lung disease lacking specific therapeutics.Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme of nicotinamide adenine dinucleotide (NAD) salvage biosynthesis pathway and a cytokine, has been previously reported as biomarker for diseases; however, role NAMPT in not elucidated.Methods: We identified level changes by analyzing public RNA-Seq databases, verified collected clinical samples mice model Western blotting, qRT-PCR, ELISA Immunohistochemical staining.We investigated mechanism using pharmacological inhibition on Nampt transgenic mice.In vivo macrophage depletion clodronate liposomes reinfusion IL-4-induced M2 bone marrow-derived macrophages (BMDMs) from wild-type mice, combined with vitro cell experiments, were performed to further validate underlying involving fibrosis.Results: found that increased lungs patients IPF bleomycin (BLM)-induced fibrosis.NAMPT inhibitor FK866 alleviated BLM-induced significantly reduced levels bronchoalveolar lavage fluid (BALF).The single-cell RNA sequencing showed expression monocytes/macrophages was much higher than other cells.Knocking out mouse (Nampt fl/fl ;Cx3cr1 CreER ) decreased BALF, infiltration improved survival.Depleting subsequent BMDMs reversed protective effect monocyte/macrophage NAMPT-deletion fibrosis.In experiments confirmed engaged related released promoting polarization non-enzyme-dependent manner activating STAT6 signal pathway.Conclusions: prompts bleomycin-induced driving mice.Targeting promising strategy treating fibrosis.

Language: Английский

Citations

9
Traffic-related air pollution (TRAP) exposure, lung function, airway inflammation and expiratory microbiota: A randomized crossover study DOI Creative Commons

Rongrong Xu,

Yanping Zhang, Tingting Wu

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2025, Volume and Issue: 289, P. 117545 - 117545

Published: Jan. 1, 2025

Language: Английский

Citations

1
NAT10 accelerates pulmonary fibrosis through N4-acetylated TGFB1-initiated epithelial-to-mesenchymal transition upon ambient fine particulate matter exposure DOI Creative Commons

Shenshen Wu,

Lijia Yin,

Ke Han

et al.

Environmental Pollution, Journal Year: 2023, Volume and Issue: 322, P. 121149 - 121149

Published: Jan. 30, 2023

Language: Английский

Citations

21
The effect of real-ambient PM2.5 exposure on the lung and gut microbiomes and the regulation of Nrf2 DOI Creative Commons
Jianxin Wang,

Yongwei Yan,

Honglin Si

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2023, Volume and Issue: 254, P. 114702 - 114702

Published: March 2, 2023

The influence of air pollution on human health has sparked widespread concerns across the world. Previously, we found that exposure to ambient fine particulate matter (PM2.5) in our "real-ambient exposure" system can result reduced lung function. However, mechanism organ-specific toxicity is still not fully elucidated. balance microbiome contributes maintaining and gut health, but changes under PM2.5 are understood. Recently, crosstalk between nuclear factor E2-related 2 (Nrf2) was reported. it unclear whether Nrf2 affects microbiomes exposure. In this study, wild-type (WT) Nrf2-/- (KO) mice were exposed filtered (FA) real (PM) " real-ambient examine microbiomes. Here, data suggested dysbiosis KO exposure, ameliorated disorder. Our study demonstrated detrimental impacts by inhaled supported protective role homeostasis

Language: Английский

Citations

20
A multi-omics investigation of the lung injury induced by PM2.5 at environmental levels via the lung-gut axis DOI
Shuiping Dai, Zhenglu Wang, Min Cai

et al.

The Science of The Total Environment, Journal Year: 2024, Volume and Issue: 926, P. 172027 - 172027

Published: March 27, 2024

Language: Английский

Citations

6
Potential targeted therapy based on deep insight into the relationship between the pulmonary microbiota and immune regulation in lung fibrosis DOI Creative Commons
Tao Zhang, Min Zhang, Liqing Yang

et al.

Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14

Published: Jan. 24, 2023

Pulmonary fibrosis is an irreversible disease, and its mechanism unclear. The lung a vital organ connecting the respiratory tract outside world. changes in microbiota affect progress of fibrosis. latest research showed that differs healthy people, including idiopathic pulmonary (IPF) acute exacerbation-idiopathic (AE-IPF). How to regulate whether potential regulatory can become necessary targeted treatment IPF are Some studies immune response balance maintain homeostasis. However, unbalanced homeostasis stimulates response. subsequent biological effects closely related Core fucosylation (CF), significant protein functional modification, affects microbiota. CF regulates modifications by regulating key inflammatory factors signaling pathways generated after regulation, such as antibiotic treatment, vitamin D supplementation, exosome micro-RNAs, has achieved initial effect clearing storm induced Based on above, highlight this review clarifying relationship between regulation identifying correlation two, impact fibrosis, therapeutic targets.

Language: Английский

Citations

13
Pirfenidone Alleviates Against Fine Particulate Matter-Induced Pulmonary Fibrosis Modulating via TGF-β1/TAK1/MKK3/p38 MAPK Signaling Pathway in Rats DOI Creative Commons
Jun-Seok Sung, Il‐Gyu Ko, Lakkyong Hwang

et al.

Biomedicines, Journal Year: 2025, Volume and Issue: 13(4), P. 989 - 989

Published: April 17, 2025

Increased exposure to particulate matter (PM) from air pollution causes lung inflammation and increases morbidity mortality due respiratory diseases. Pirfenidone is an anti-fibrotic agent used treat idiopathic pulmonary fibrosis. Background/Objectives: In this experiment, we studied the therapeutic effects of pirfenidone on PM-induced Methods: Pulmonary fibrosis was induced by intratracheal application 100 μg/kg PM10 mixed with 200 μL saline. After 42 days infusion, 0.2 mL distilled water orally administered pirfenidone-treated groups (200 400 mg/kg) every other day for a total 15 times over 30 days. Results: The administration PM resulted in injury significant decrease number bronchoalveolar lavage fluid cells. increased score, level fibrosis, production pro-inflammatory cytokines. treatment effectively suppressed transforming growth factor-β-activated kinase 1 present changes inhibited expressions mitogen-activated protein 3 p38, which factor-β, ultimately alleviating upregulated fibronectin type collagen. enhanced connective tissue factor hydroxyproline levels tissue. these fibrosis-related factors were treatment. Conclusions: These results suggest that therapeutically effective against

Language: Английский

Citations

0
The role of PD-1/PD-L1 axis in idiopathic pulmonary fibrosis: Friend or foe? DOI Creative Commons
Aimin Jiang, Na Liu, Jingjing Wang

et al.

Frontiers in Immunology, Journal Year: 2022, Volume and Issue: 13

Published: Dec. 5, 2022

Idiopathic pulmonary fibrosis (IPF) is a devastating interstitial lung disease with bleak prognosis. Mounting evidence suggests that IPF shares bio-molecular similarities cancer. Given the deep understanding of programmed cell death-1 (PD-1)/programmed death-ligand 1 (PD-L1) pathway in cancer immunity and successful application immune checkpoint inhibitors (ICIs) cancer, recent studies have noticed role PD-1/PD-L1 axis IPF. However, conclusions are ambiguous, latent mechanisms remain unclear. In this review, we will summarize based on current murine models clinical studies. We found plays more predominant profibrotic than its immunomodulatory by interacting multiple types pathways. Most preclinical also indicated blockade could attenuate severity mice models. This review bring significant insights into identifying new therapeutic targets.

Language: Английский

Citations

16