scholarly journals IL‐17A‐producing T cells exacerbate fine particulate matter‐induced lung inflammation and fibrosis by inhibiting PI3K/Akt/mTOR‐mediated autophagy

2020 ◽  
Vol 24 (15) ◽  
pp. 8532-8544 ◽  
Author(s):  
Lu‐Hong Cong ◽  
Tao Li ◽  
Hui Wang ◽  
Yi‐Na Wu ◽  
Shu‐Peng Wang ◽  
...  
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.


2016 ◽  
Vol 32 (4) ◽  
pp. 1121-1134 ◽  
Author(s):  
Yuefei Jin ◽  
Weidong Wu ◽  
Weiguo Zhang ◽  
Yang Zhao ◽  
Yongjun Wu ◽  
...  

2018 ◽  
Vol 295 ◽  
pp. S181
Author(s):  
M. Al Zallouha ◽  
S. Billet ◽  
Y. Landkocz ◽  
M. Borgie ◽  
S. Poddighe ◽  
...  

2021 ◽  
Vol 219 ◽  
pp. 112351
Author(s):  
Juan Li ◽  
Zhen An ◽  
Jie Song ◽  
Jinge Du ◽  
Lin Zhang ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Mengmeng Xu ◽  
Yanbei Zhang ◽  
Muyun Wang ◽  
Hai Zhang ◽  
Yuqing Chen ◽  
...  

Exposure to fine particulate matter (PM2.5) has been associated with lung inflammation and airway hyperresponsiveness (AHR). Transient receptor potential (TRP) vanilloid 1 (TRPV1) and ankyrin 1 (TRPA1) both may play important roles in lung inflammation and AHR. We investigated whether PM2.5-induced lung inflammation and AHR could be prevented by blocking TRPV1 and TRPA1 channels. Mice were injected intraperitoneally with AMG9810 (30 mg/kg, a TRPV1 antagonist) or A967079 (30 mg/kg, a TRPA1 antagonist) or their combination or vehicle (PBS) one hour before intranasal instillation of PM2.5 (7.8 mg/kg) or vehicle (PBS) for two consecutive days, and then the mice were studied 24 h later. All pretreatments inhibited PM2.5-induced AHR and inflammatory infiltration in the lung tissue and decreased inflammatory cytokine levels in the bronchoalveolar lavage fluid, together with oxidant levels in the lung. AMG9810 inhibited MFF expression and increased MFN2 expression while A967079 inhibited DRP1 expression and increased OPA1 expression; combined pretreatment reduced MFF and DPR1 expression and increased MFN2 and OPA1 expression. All pretreatments inhibited the activation of the TLR4/NF-κB pathway, while A967079 alone, and combined with AMG9810 also reduced the activation of the NLRP3/caspase-1 pathway. Both TRPV1 and TRPA1 channels play an important role in PM2.5-induced lung inflammation and AHR. However, inhibition of the TRPA1 channel or combined inhibition of TRPA1 and TRPV1 channels resulted in greater inhibitory effect on PM2.5-induced lung injury through regulating the mitochondrial fission/fusion proteins and inhibiting the TLR4/NF-κB and NLRP3/caspase-1 pathways.


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

2021 ◽  
pp. 106386
Author(s):  
Heyu Yin ◽  
Sina Parsnejad ◽  
Ehsan Ashoori ◽  
Hao Wan ◽  
Wen Li ◽  
...  

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