Tags

Type your tag names separated by a space and hit enter

Particulate matter exposure promotes Pseudomonas aeruginosa invasion into airway epithelia by upregulating PAFR via the ROS-mediated PI3K pathway.
Hum Cell. 2020 Oct; 33(4):963-973.HC

Abstract

Over exposure to particulate matter (PM) could irritate respiratory tract infection; while, Pseudomonas aeruginosa (P. aeruginosa) is one of the main common pathogens. Our study aims are to define whether PM exposure enhances the invasion of P. aeruginosa into the airway epithelia and to characterize the underlying mechanisms. Human bronchial epithelial cells (BEAS-2B) or BEAS-2B transfected by PAFR siRNA were challenged with PM and pretreated with N-acetylcysteine (NAC), LY294002 (PI3K inhibitor), BAY 11-7082 (NF-κB inhibitor), or CV-3988 (PAFR antagonist). P. aeruginosa invasion was evaluated using colony-forming units assay and confocal microscopy. Real-time RT-PCR, immunofluorescence, flow cytometry and western blotting were used to detect the genes or proteins expression. PM exposure promoted P. aeruginosa invasion into BEAS-2B cells through ROS-mediated PI3K pathway which enhanced the expression of PAFR, which could be alleviated by treatment with NAC, LY294002, and BAY 11-7082. Furthermore, NAC and PAFR siRNA attenuated PM-stimulated activation of PI3K pathway. Treatment with PAFR antagonist and siRNA also alleviated PM exposure-induced P. aeruginosa invasion into BEAS-2B cells. Our results demonstrated that PM exposure increased the PAFR expression and activated the PI3K pathway in a ROS-dependent manner. Upregulated PAFR and activated PI3K pathway formed a positive regulatory loop and promoted the invasion of P. aeruginosa into airway epithelia. These mechanisms may provide a novel approach against P.aeruginosa invasion.

Links

Publisher Full Text (DOI)

Authors+Show Affiliations

Liu J
Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.
Chen X
Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.
Zhou J
Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.
Ye L
Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.
Yang D
Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China. yang.dong@zs-hospital.sh.cn.
Song Y
Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, 180 Fenglin Road, Shanghai, 200032, People's Republic of China. ylsong70@163.com. Department of Respiratory Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, People's Republic of China. ylsong70@163.com. Department of Pulmonary Medicine, Zhongshan Hospital, Qingpu Branch, Shanghai, People's Republic of China. ylsong70@163.com.

MeSH

Cell LineEpithelial CellsHumansParticulate MatterPhosphatidylinositol 3-KinasesPlatelet Membrane GlycoproteinsPseudomonas aeruginosaReactive Oxygen SpeciesReceptors, G-Protein-CoupledRespiratory MucosaSignal TransductionUp-Regulation

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32627147

Citation

Liu, Jinguo, et al. "Particulate Matter Exposure Promotes Pseudomonas Aeruginosa Invasion Into Airway Epithelia By Upregulating PAFR Via the ROS-mediated PI3K Pathway." Human Cell, vol. 33, no. 4, 2020, pp. 963-973.
Liu J, Chen X, Zhou J, et al. Particulate matter exposure promotes Pseudomonas aeruginosa invasion into airway epithelia by upregulating PAFR via the ROS-mediated PI3K pathway. Hum Cell. 2020;33(4):963-973.
Liu, J., Chen, X., Zhou, J., Ye, L., Yang, D., & Song, Y. (2020). Particulate matter exposure promotes Pseudomonas aeruginosa invasion into airway epithelia by upregulating PAFR via the ROS-mediated PI3K pathway. Human Cell, 33(4), 963-973. https://doi.org/10.1007/s13577-020-00378-y
Liu J, et al. Particulate Matter Exposure Promotes Pseudomonas Aeruginosa Invasion Into Airway Epithelia By Upregulating PAFR Via the ROS-mediated PI3K Pathway. Hum Cell. 2020;33(4):963-973. PubMed PMID: 32627147.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Particulate matter exposure promotes Pseudomonas aeruginosa invasion into airway epithelia by upregulating PAFR via the ROS-mediated PI3K pathway. AU - Liu,Jinguo, AU - Chen,Xiaoyan, AU - Zhou,Jian, AU - Ye,Ling, AU - Yang,Dong, AU - Song,Yuanlin, Y1 - 2020/07/05/ PY - 2019/08/08/received PY - 2020/05/14/accepted PY - 2020/7/7/pubmed PY - 2020/10/28/medline PY - 2020/7/7/entrez KW - Oxidative stress KW - Particulate matter KW - Platelet-activating factor receptor KW - Pseudomonas aeruginosa SP - 963 EP - 973 JF - Human cell JO - Hum Cell VL - 33 IS - 4 N2 - Over exposure to particulate matter (PM) could irritate respiratory tract infection; while, Pseudomonas aeruginosa (P. aeruginosa) is one of the main common pathogens. Our study aims are to define whether PM exposure enhances the invasion of P. aeruginosa into the airway epithelia and to characterize the underlying mechanisms. Human bronchial epithelial cells (BEAS-2B) or BEAS-2B transfected by PAFR siRNA were challenged with PM and pretreated with N-acetylcysteine (NAC), LY294002 (PI3K inhibitor), BAY 11-7082 (NF-κB inhibitor), or CV-3988 (PAFR antagonist). P. aeruginosa invasion was evaluated using colony-forming units assay and confocal microscopy. Real-time RT-PCR, immunofluorescence, flow cytometry and western blotting were used to detect the genes or proteins expression. PM exposure promoted P. aeruginosa invasion into BEAS-2B cells through ROS-mediated PI3K pathway which enhanced the expression of PAFR, which could be alleviated by treatment with NAC, LY294002, and BAY 11-7082. Furthermore, NAC and PAFR siRNA attenuated PM-stimulated activation of PI3K pathway. Treatment with PAFR antagonist and siRNA also alleviated PM exposure-induced P. aeruginosa invasion into BEAS-2B cells. Our results demonstrated that PM exposure increased the PAFR expression and activated the PI3K pathway in a ROS-dependent manner. Upregulated PAFR and activated PI3K pathway formed a positive regulatory loop and promoted the invasion of P. aeruginosa into airway epithelia. These mechanisms may provide a novel approach against P.aeruginosa invasion. SN - 1749-0774 UR - https://www.unboundmedicine.com/medline/citation/32627147/Particulate_matter_exposure_promotes_Pseudomonas_aeruginosa_invasion_into_airway_epithelia_by_upregulating_PAFR_via_the_ROS_mediated_PI3K_pathway_ DB - PRIME DP - Unbound Medicine ER -