尽管卡斯巴酶激活,但维布里奥帕拉海莫利蒂克斯热稳定直接血解素诱导非经典的编程细胞死亡
Pratima Verma1, Aakanksha Chauhan1, Reena Thakur1
1Department of Biological Sciences, Indian Institute of Science Education and Research Mohali, Mohali, Punjab, India.
Molecular microbiology
|October 11, 2023
概括
来自Vibrio parahaemolyticus的热稳定直接血清素 (TDH) 通过破坏线粒体,触发了类似细胞灭绝的细胞死亡. 这种毒素诱导了酶独立的细胞死亡,揭示了对宿主-病原体相互作用的新见解.
科学领域:
- 微生物学 微生物学
- 细胞生物学 细胞生物学
- 毒理学 毒理学 毒理学
背景情况:
- 热稳定直接血液溶解素 (TDH) 是Vibrio parahaemolyticus的主要毒性因子.
- TDH是一种形成毛孔的毒素,引起细胞毒性,但其细胞死亡机制尚未完全理解.
研究的目的:
- 阐明TDH诱导的细胞死亡的机制细节.
- 调查体,线粒体和其他介质在TDH诱导的细胞毒性中的作用.
主要方法:
- 使用了Caco-2肠上皮细胞和THP-1单细胞.
- 分析了酶激活,XIAP,Smac/Diablo水平,线粒体损伤以及AIF和内核酶G的释放.
- 评估了ROS和PARP-1在TDH介导的细胞死亡中的作用.
主要成果:
- 在这两种细胞类型中,TDH诱导了类似亡的细胞死亡特征.
- 观察到酶激活,但细胞死亡在很大程度上与酶无关,可能是由于XIAP/Smac-Diablo水平的改变.
- 线粒体损伤和AIF/内核酶G的释放是TDH诱导细胞死亡的关键事件.
- 在特定的细胞类型中,ROS和PARP-1发挥了重要的作用.
结论:
- TDH诱导了一种非经典的编程细胞死亡途径,以线粒体损伤为中心.
- 这项研究揭示了在TDH介导的宿主细胞死亡中分子的复杂相互作用.
- 这些发现提高了对TDH在Vibrio parahaemolyticus病原和宿主-病原体相互作用中的作用的理解.
相关概念视频
Overview of Cell Death
7.3K
Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
7.3K
Autophagic Cell Death
3.4K
Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
3.4K
Necrosis
4.6K
Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
4.6K
The Extrinsic Apoptotic Pathway
6.4K
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
6.4K
Apoptosis
11.5K
Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
11.5K
The Intrinsic Apoptotic Pathway
6.6K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
6.6K


