Effects of high-tidal-volume mechanical ventilation on the expression of P2X7 receptor and inflammatory response in lung tissue of rats

被引:2
作者
Jia, Jia [1 ]
Qin, Hanyu [1 ]
Zang, Bin [1 ]
机构
[1] China Med Univ, Shengjing Hosp, Intens Care Unit, 36 Sanhao St, Shenyang 110004, Liaoning, Peoples R China
关键词
inflammatory mediator; mechanical ventilation; P2X7; receptor; ventilator-induced lung injury; NLRP3; INFLAMMASOME; ALVEOLAR MACROPHAGES; INJURY; ACTIVATION; SUPPRESSION; CONTRIBUTES;
D O I
10.1177/2058739218795945
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Ventilator-induced lung injury is a severe complication mainly caused from mechanical ventilation (MV), associated with the upregulation of inflammation response. The mechanism still remains unclear. This study aims to explore the effects of pathological damage, neutrophil infiltration, expression of P2X7 receptor, and activation of Caspase-1 in lung tissue using a rat model. Sprague Dawley (SD) rats were randomly divided into sham group, conventional MV group, and high-tidal-volume ventilation group and fed with clean water and rat food. The sham group received tracheotomy without MV; conventional MV group was given 7 mL/kg tidal volume ventilation, and high-tidal-volume MV group was given 28 mL/kg tidal volume ventilation. All the rats were sacrificed after 4 h of ventilation or spontaneous breath. Lung wet/dry ratio was measured, and paraffin sections were prepared for pathological injury assessment and immunohistochemistry of P2X7 and myeloperoxidase levels. Lung homogenate was used for Western blot analysis of P2X7 receptor and Caspase-1 levels and real-time polymerase chain reaction (PCR) analysis of P2X7 gene expression level. Compared to sham group and conventional MV group, high-tidal-volume MV led to an increase in lung wet/dry ratio and histology score. High-tidal-volume ventilation also led to chemotaxis of neutrophils. The expression levels of protein and messenger RNA (mRNA) of P2X7 receptor were significantly upregulated. Cleaved-caspase-1 expression was also upregulated. All data provide the evidence that high-tidal-volume MV can lead to lung injury, neutrophils infiltration, and upregulation of cleaved-Caspase-1 level. This result may be related to the upregulation of P2X7 receptor expression.
引用
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页码:1 / 7
页数:7
相关论文
共 17 条
[1]  
Ather Jennifer L, 2014, J Environ Immunol Toxicol, V1, P108
[2]   Suppression of P2X7/NF-κB pathways by Schisandrin B contributes to attenuation of lipopolysaccharide-induced inflammatory responses in acute lung injury [J].
Cai, Zhiyong ;
Liu, Jindi ;
Bian, Hongliang ;
Cai, Jinlan ;
Zhu, Gendi .
ARCHIVES OF PHARMACAL RESEARCH, 2016, 39 (04) :499-507
[3]   Mechanical ventilation modulates Toll-like receptors 2, 4, and 9 on alveolar macrophages in a ventilator-induced lung injury model [J].
Dai, Huijun ;
Pan, Linghui ;
Lin, Fei ;
Ge, Wanyun ;
Li, Wei ;
He, Sheng .
JOURNAL OF THORACIC DISEASE, 2015, 7 (04) :616-624
[4]   The P2X7 receptor directly interacts with the NLRP3 inflammasome scaffold protein [J].
Franceschini, Alessia ;
Capece, Marina ;
Chiozzi, Paola ;
Falzoni, Simonetta ;
Sanz, Juana Maria ;
Sarti, Alba Clara ;
Bonora, Massimo ;
Pinton, Paolo ;
Di Virgilio, Francesco .
FASEB JOURNAL, 2015, 29 (06) :2450-2461
[5]   Deletion of P2X7 attenuates hyperoxia-induced acute lung injury via inflammasome suppression [J].
Galam, Lakshmi ;
Rajan, Ashna ;
Failla, Athena ;
Soundararajan, Ramani ;
Lockey, Richard F. ;
Kolliputi, Narasaiah .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 2016, 310 (06) :L572-L581
[6]   Transient P2X7 Receptor Activation Triggers Macrophage Death Independent of Toll-like Receptors 2 and 4, Caspase-1, and Pannexin-1 Proteins [J].
Hanley, Peter J. ;
Kronlage, Moritz ;
Kirschning, Carsten ;
del Rey, Adriana ;
Di Virgilio, Francesco ;
Leipziger, Jens ;
Chessell, Iain P. ;
Sargin, Sarah ;
Filippov, Mikhail A. ;
Lindemann, Otto ;
Mohr, Simon ;
Koenigs, Volker ;
Schillers, Hermann ;
Baehler, Martin ;
Schwab, Albrecht .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2012, 287 (13) :10650-10663
[7]   K+ Efflux Agonists Induce NLRP3 Inflammasome Activation Independently of Ca2+ Signaling [J].
Katsnelson, Michael A. ;
Rucker, L. Graham ;
Russo, Hana M. ;
Dubyak, George R. .
JOURNAL OF IMMUNOLOGY, 2015, 194 (08) :3937-+
[8]   Ventilator-induced Lung Injury Is Mediated by the NLRP3 Inflammasome [J].
Kuipers, Maria T. ;
Aslami, Hamid ;
Janczy, John R. ;
van der Sluijs, Koenraad F. ;
Vlaar, Alexander P. J. ;
Wolthuis, Esther K. ;
Choi, Goda ;
Roelofs, Joris J. T. H. ;
Flavell, Richard A. ;
Sutterwala, Fayyaz S. ;
Bresser, Paul ;
Leemans, Jaklien C. ;
van der Poll, Tom ;
Schultz, Marcus J. ;
Wieland, Catharina W. .
ANESTHESIOLOGY, 2012, 116 (05) :1104-1115
[9]   Regulation and Function of the Nucleotide Binding Domain Leucine-Rich Repeat-Containing Receptor, Pyrin Domain-Containing-3 Inflammasome in Lung Disease [J].
Lee, Seonmin ;
Suh, Gee-Young ;
Ryter, Stefan W. ;
Choi, Augustine M. K. .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2016, 54 (02) :151-160
[10]   A Critical Role for P2X7 Receptor-Induced VCAM-1 Shedding and Neutrophil Infiltration during Acute Lung Injury [J].
Mishra, Amarjit ;
Guo, Yujie ;
Zhang, Li ;
More, Sunil ;
Weng, Tingting ;
Chintagari, Narendranath Reddy ;
Huang, Chaoqun ;
Liang, Yurong ;
Pushparaj, Samuel ;
Gou, Deming ;
Breshears, Melanie ;
Liu, Lin .
JOURNAL OF IMMUNOLOGY, 2016, 197 (07) :2828-2837