Molecular Mechanism of the Cell Membrane Pore Formation Induced by Bubble Stable Cavitation

2018 ◽  
Vol 123 (1) ◽  
pp. 71-78 ◽  
Author(s):  
Viet Hoang Man ◽  
Phan Minh Truong ◽  
Mai Suan Li ◽  
Junmei Wang ◽  
Nguyen-Thi Van-Oanh ◽  
...  
2019 ◽  
Vol 21 (10) ◽  
pp. 5578-5585 ◽  
Author(s):  
Rudramani Pokhrel ◽  
Elumalai Pavadai ◽  
Bernard S. Gerstman ◽  
Prem P. Chapagain

The Ebola virus delta peptide homo-oligomerizes in the host cell membrane to form amphipathic pores that alter the membrane properties.


2020 ◽  
Author(s):  
Chunlan Shan ◽  
Shushu Miao ◽  
Chaoying Liu ◽  
Weiwei Zhao ◽  
Bo Zhang ◽  
...  

Abstract Background In this study we evaluated the molecular mechanism by which pyroptosis is induced in mononuclear macrophages isolated from Saba pigs following infection with pathogenic E. coli high pathogenicity island (HPI). Mononuclear macrophages were divided into four treatment groups: control, Lipopolysaccharide (LPS) + adenosine triphosphate (ATP), HPI positive (+) strain and HPI negative (-) strain. The mononuclear macrophages and their culture supernatants were collected at 0.5, 3, 6, 9, 12 and 24 h after infection. DNA changes were detected by TUNEL staining and the integrity of the cell membrane was evaluated by propidium iodide (PI) staining. Changes in mRNA expression levels of NLRP3, caspase-1, IL-1β, and IL-18 gene in mononuclear macrophages were analyzed by quantitative real-time polymerase chain reaction (RT-PCR) and caspase-1 protein expression was detected by indirect immunofluorescence. IL-1β and IL-18 concentration in the mononuclear macrophage culture supernatant were measured by ELISA. Results Compared with the control group, TUNEL and PI staining of mononuclear macrophages was significantly increased following infection with the HPI + /HPI - strains ( P < 0.01 or P < 0.05), with significantly higher levels detected in the HPI + group compared with those in the HPI - group ( P < 0.01 and P < 0.05). Compared with the control group, the expression levels of NLRP3, caspase-1, IL-1β, and IL-18 in the HPI groups were upregulated after pathogenic E. coli infection, with significantly higher levels detected in the HPI + group compared with those in the HPI - group ( P < 0.01 or P < 0.05). Conclusions These findings showed that pathogenic E. coli HPI infection of Saba pigs results induced pyroptosis of mononuclear macrophages characterized by increased expression of NLRP3, caspase-1, IL-1β and IL-18 mRNA in mononuclear macrophages, the induction of cell membrane pore formation, nuclear DNA damage, and the secretion of IL-1β and IL-18 to enhance the inflammatory response.


2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Chunlan Shan ◽  
Shushu Miao ◽  
Chaoying Liu ◽  
Bo Zhang ◽  
Weiwei Zhao ◽  
...  

Abstract Background Pyroptosis plays a pivotal role in the pathogenesis of many inflammatory diseases. The molecular mechanism by which pyroptosis is induced in macrophages following infection with pathogenic E. coli high pathogenicity island (HPI) will be evaluated in our study. Results After infection with the HPI+/HPI− strains and LPS, decreased macrophage cell membrane permeability and integrity were demonstrated with propidium iodide (PI) staining and the lactate dehydrogenase (LDH) assay. HPI+/HPI−-infection was accompanied by upregulated expression levels of NLRP3, ASC, caspase-1, IL-1β, IL-18 and GSDMD, with significantly higher levels detected in the HPI+ group compared to those in the HPI− group (P < 0.01 or P < 0.05). HPI+ strain is more pathogenic than HPI− strain. Conclusion Our findings indicate that pathogenic E. coli HPI infection of Saba pigs causes pyroptosis of macrophages characterized by upregulated expression of pyroptosis key factors in the NLRP3/ASC/caspase-1 signaling pathway, direct cell membrane pore formation, and secretion of the inflammatory factor IL-1β and IL-18 downstream of NLRP3 and caspase-1 activation to enhance the inflammatory response.


2014 ◽  
Vol 39 (11) ◽  
pp. 510-516 ◽  
Author(s):  
Robert J.C. Gilbert ◽  
Mauro Dalla Serra ◽  
Christopher J. Froelich ◽  
Mark I. Wallace ◽  
Gregor Anderluh
Keyword(s):  

Biochemistry ◽  
2012 ◽  
Vol 51 (46) ◽  
pp. 9406-9419 ◽  
Author(s):  
Suren A. Tatulian ◽  
Pranav Garg ◽  
Kathleen N. Nemec ◽  
Bo Chen ◽  
Annette R. Khaled

2018 ◽  
Vol 5 (2) ◽  
pp. 780-794 ◽  
Author(s):  
Neha Awasthi ◽  
Wojciech Kopec ◽  
Natalia Wilkosz ◽  
Dorota Jamróz ◽  
Jochen S. Hub ◽  
...  

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