The Effect of Fine Particulate Matter on the Inflammatory Responses in Human Upper Airway Mucosa

2019 ◽  
Vol 200 (10) ◽  
pp. 1315-1318 ◽  
Author(s):  
Hui Qing ◽  
Xiangdong Wang ◽  
Nan Zhang ◽  
Kaili Zheng ◽  
Kun Du ◽  
...  
2014 ◽  
Vol 2014 ◽  
pp. 1-14 ◽  
Author(s):  
Wen-cai Zhang ◽  
Yan-ge Wang ◽  
Zheng-feng Zhu ◽  
Fang-qin Wu ◽  
Yu-dong Peng ◽  
...  

Objective. To investigate the role of CD4+CD25+T cells (Tregs) in protecting fine particulate matter (PM-) induced inflammatory responses, and its potential mechanisms.Methods. Human umbilical vein endothelial cells (HUVECs) were treated with graded concentrations (2, 5, 10, 20, and 40 µg/cm2) of suspension of fine particles for 24h. For coculture experiment, HUVECs were incubated alone, with CD4+CD25−T cells (Teff), or with Tregs in the presence of anti-CD3 monoclonal antibodies for 48 hours, and then were stimulated with or without suspension of fine particles for 24 hours. The expression of adhesion molecules and inflammatory cytokines was examined.Results. Adhesion molecules, including vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1), and inflammatory cytokines, such as interleukin (IL-) 6 and IL-8, were increased in a concentration-dependent manner. Moreover, the adhesion of human acute monocytic leukemia cells (THP-1) to endothelial cells was increased and NF-κB activity was upregulated in HUVECs after treatment with fine particles. However, after Tregs treatment, fine particles-induced inflammatory responses and NF-κB activation were significantly alleviated. Transwell experiments showed that Treg-mediated suppression of HUVECs inflammatory responses impaired by fine particles required cell contact and soluble factors.Conclusions. Tregs could attenuate fine particles-induced inflammatory responses and NF-κB activation in HUVECs.


2020 ◽  
Vol 328 ◽  
pp. 52-60 ◽  
Author(s):  
Wanjun Yuan ◽  
Ciara C. Fulgar ◽  
Xiaolin Sun ◽  
Christoph F.A. Vogel ◽  
Ching-Wen Wu ◽  
...  

2015 ◽  
Vol 237 (3) ◽  
pp. 174-180 ◽  
Author(s):  
Hsiao-Chi Chuang ◽  
Kin-Fai Ho ◽  
Jun-Ji Cao ◽  
Kai-Jen Chuang ◽  
Steven Sai Hang Ho ◽  
...  

2016 ◽  
Vol 36 (2) ◽  
pp. 165-173 ◽  
Author(s):  
Ruijin Li ◽  
Lifang Zhao ◽  
Jinlong Tong ◽  
Yuchao Yan ◽  
Chong Xu

Fine particulate matter (PM2.5) and sulfur dioxide (SO2) are 2 common air pollutants, but their toxicological effects of coexposure are still not fully clear. In this study, SO2 exposure (5.6 mg/m3) couldn’t cause obvious inflammatory responses in rat lungs. The PM2.5 exposure (1.5 mg/kg body weight) increased inflammatory cell counts in bronchoalveolar lavage fluid (BALF) and some inflammation damage. Importantly, SO2 and PM2.5 (1.5, 6.0, and 24.0 mg/kg) coexposure induced pathological and ultrastructural damage and raised inflammatory cells in BALF compared with the control. Also, they significantly elevated the levels of pro-inflammatory cytokines, adhesion molecule, and nitric oxide (NO) and promoted the gene expression of nuclear factor kappa B (NF-κB), phosphorylated p38 (p-p38), and Toll-like receptor 4 (TLR4) in rat lungs treated with higher dose of PM2.5 (6.0 and 24.0 mg/kg) plus SO2 relative to the control or SO2 group, along with the decreased inhibitor of NF-κBα and increased inhibitor of NF-κB kinase β expressions. The changes in the inflammatory markers in the presence of PM2.5 plus SO2 were not significant compared with the PM2.5 group. The results indicated that inflammatory injury and pathological and ultrastructural damage in rat lungs exposed to PM2.5 plus SO2 were involved in TLR4/p38/NF-κB pathway activation accompanied by oversecretion of pro-inflammatory cytokine, adhesion molecule, and NO. It provides more useful evidence to understand the possible toxicological mechanism that PM2.5 and SO2 copollution exacerbate lung disease.


2019 ◽  
Vol 35 (10) ◽  
pp. 670-678 ◽  
Author(s):  
Yifei Le ◽  
Xiao Hu ◽  
Ji Zhu ◽  
Cui Wang ◽  
Zhen Yang ◽  
...  

This study aims to investigate the role of Toll-like receptors (TLRs) on fine particulate matter (PM2.5)-induced inflammatory responses of vascular endothelial cells. Inflammatory factors and TLRs were examined in the aorta of mice after nonsurgical intratracheal instillation of PM2.5 as well as in the human umbilical vein endothelial cells (HUVECs) treated with PM2.5. In addition, the effects of TLR2 and TLR4 inhibitors in the secretion of interleukin 6 (IL-6) and IL-1β and the expression of TLRs were determined in the HUVECs. The results showed that PM2.5 could increase the expression of IL-1β, IL-6, TLR2, and TLR4 in vitro and in vivo. Anti-TLR2 IgG or TAK242, an inhibitor of TLR4, decreased the secretion of IL-1β and IL-6 by HUVECs and reduced the expression of corresponding TLRs. In conclusion, we demonstrate that both TLR2 and TLR4 are involved in PM2.5-induced inflammatory responses of vascular endothelial cells. Inhibition of TLR2 and TLR4 expression has the potential to prevent PM2.5-induced cardiovascular diseases.


2020 ◽  
Author(s):  
Yazhen Gong ◽  
Shanjun Li ◽  
Nicholas Sanders ◽  
Guang Shi

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