scholarly journals Mycobacterium tuberculosis PPE32 promotes cytokines production and host cell apoptosis through caspase cascade accompanying with enhanced ER stress response

Oncotarget ◽  
2016 ◽  
Vol 7 (41) ◽  
pp. 67347-67359 ◽  
Author(s):  
Wanyan Deng ◽  
Wenmin Yang ◽  
Jie Zeng ◽  
Abualgasim Elgaili Abdalla ◽  
Jianping Xie
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Stress Response ◽  
Er Stress ◽  
Host Cell ◽  
Cell Apoptosis ◽  
Er Stress Response ◽  
Host Cell Apoptosis ◽  
Caspase Cascade

Inhibition of host cell apoptosis by Toxoplasma gondii is accompanied by reduced activation of the caspase cascade and alterations of poly(ADP-ribose) polymerase expression

2001 ◽  
Vol 114 (19) ◽  
pp. 3495-3505
Author(s):  
Stefan Goebel ◽  
Uwe Gross ◽  
Carsten G. K. Lüder
Keyword(s):  
Toxoplasma Gondii ◽  
Cytochrome C ◽  
Host Cell ◽  
Cell Apoptosis ◽  
Mrna Levels ◽  
U937 Cells ◽  
Cytochrome C Release ◽  
Protein Levels ◽  
Host Cell Apoptosis ◽  
Caspase Cascade

The obligate intracellular protozoan parasite Toxoplasma gondii has been shown to protect different cell types from apoptosis induced by a variety of pro-apoptotic treatments. However, the precise cell biological mechanisms of this inhibition remained unknown. As shown in this study, apoptosis in human-derived HL-60 and U937 cells induced by treatment with actinomycin D or TNF-α in combination with cycloheximide, respectively, was indeed dose-dependently downregulated by prior infection with T. gondii, as determined by DNA fragmentation assays. Cleavage of caspase 3 and caspase 9 after treatment with pro-apoptotic stimuli was considerably diminished by T. gondii. Furthermore, release of mitochondrial cytochrome c during apoptosis in HL-60 cells was prevented by intracellular parasites and this was correlated with the absence of DNA strand breaks on the single cell level. Inhibition of cytochrome c release coincided with a twofold upregulation of Mcl-1 protein levels in HL-60 and U937 cells, while Bcl-2 expression did not increase after infection. Parasitic interference with the caspase cascade led to a reduced proteolytic cleavage of the nuclear target molecule protein kinase Cδ. In parallel, poly(ADP-ribose) polymerase protein levels were prominently downregulated by T. gondii, irrespective of whether HL-60 and U937 cells had been treated with pro-apototic stimuli or left untreated. However, poly(ADP-ribose) polymerase mRNA levels remained unchanged after infection as determined by RT-PCR analyses. These observations suggest that T. gondii has evolved different mechanisms that may contribute to downregulation of host cell apoptosis, namely inhibition of cytochrome c release and subsequent caspase activation as well as downregulation of poly(ADP-ribose) polymerase protein levels.

scholarly journals Apoptosis: Implications in Viral and Mycobacterium tuberculosis infections

2017 ◽  
Vol 5 (1) ◽  
pp. 46-57
Author(s):  
Gorakh Raj Giri ◽  
Uddhav Timilsina
Keyword(s):  
Cell Death ◽  
Mycobacterium Tuberculosis ◽  
Programmed Cell Death ◽  
Host Cell ◽  
Cell Apoptosis ◽  
Bacterial Infections ◽  
Autoimmune Disorders ◽  
Immune Defense ◽  
Pathological Conditions ◽  
Host Cell Apoptosis

Apoptosis is a form of programmed cell death leading to genetically controlled self-destruction of cells. It is essential in the development, maintenance, and regulation of cells during physiological as well as pathological conditions. Deregulation of apoptotic mechanisms is associated with various pathological diseases including cancer, autoimmune disorders, viral and bacterial infections. Virus and Mycobacterium tuberculosis elicit host cell apoptosis as a part of host immune defense or pathogen dissemination. They inhibit both extrinsic and intrinsic pathways of apoptotic mechanisms facilitating pathogen survival and escape from host immune defense.Nepal Journal of Biotechnology. Dec. 2017 Vol. 5, No. 1: 46- 57

Targeted regulation of lymphocytic ER stress response with an overall immunosuppression to alleviate allograft rejection

Biomaterials ◽  
2021 ◽  
pp. 120757
Author(s):  
Yingying Shi ◽  
Yichao Lu ◽  
Chunqi Zhu ◽  
Zhenyu Luo ◽  
Xiang Li ◽  
...  
Keyword(s):  
Stress Response ◽  
Er Stress ◽  
Allograft Rejection ◽  
Er Stress Response
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