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Functional Analysis of Genes in Mycobacterium tuberculosis Action Against Autophagosome–Lysosome Fusion
Indian Journal of Microbiology ( IF 3 ) Pub Date : 2024-03-07 , DOI: 10.1007/s12088-024-01227-4
Karthikeyan Sundaram , Leela Kagithakara Vajravelu

Abstract

Tuberculosis is a lethal disease that is one of the world's top ten death-associated infections in humans; Mycobacterium tuberculosis causes tuberculosis, and this bacterium is linked to the lysis of autophagolysosomal fusion action, a self-defense mechanism of its own. Thus, Cytoplasmic bacilli are sequestered by autophagy and transported to lysosomes to be inactivated to destroy intracellular bacteria. Besides this, a macrophage can limit intracellular Mycobacterium by using a type of autophagy, selective autophagy, a cell that marks undesirable ubiquitin existence in cytosolic cargo, acting as a “eat me” sensor in conjunction with cellular homeostasis. Mycobacterium tuberculosis genes of the PE_PGRS protein family inhibit autophagy, increase mycobacterial survival, and lead to latent tuberculosis infection associated with miRNAs. In addition, the family of autophagy-regulated (ATG) gene members are involved in autophagy and controls the initiation, expansion, maturation, and fusion of autophagosomes with lysosomes, among other signaling events that control autophagy flux and reduce inflammatory responses and forward to promote cellular proliferation. In line with the formation of caseous necrosis in macrophages by Mycobacterium tuberculosis and their action on the lysis of autophagosome fusion, it leads to latent tuberculosis infection. Therefore, we aimed to comprehensively analyses the autophagy and self-defense mechanism of Mycobacterium tuberculosis, which is to be gratified future research on novel therapeutic tools and diagnostic markers against tuberculosis.



中文翻译:

结核分枝杆菌抗自噬体-溶酶体融合作用基因的功能分析

摘要

结核病是一种致命疾病,是世界十大导致人类死亡的感染之一; 结核分枝杆菌 引起结核病,这种细菌与自噬溶酶体融合作用的裂解有关,这是其自身的一种自卫机制。因此,细胞质杆菌被自噬隔离并转运至溶酶体被灭活以破坏细胞内细菌。除此之外,巨噬细胞可以通过使用一种自噬、选择性自噬来限制细胞内分枝杆菌,选择性自噬是一种标记细胞质货物中不良泛素存在的细胞,充当与细胞稳态结合的“吃我”传感器。PE_PGRS蛋白家族的结核分枝杆菌 基因  抑制自噬,增加分枝杆菌存活率,并导致与 miRNA 相关的潜伏性结核感染。此外,自噬调节 (ATG) 基因成员家族参与自噬,控制自噬体的起始、扩增、成熟以及自噬体与溶酶体的融合,以及控制自噬流、减少炎症反应并促进炎症反应的其他信号事件。细胞增殖。与结核分枝杆菌在巨噬细胞中形成干酪样坏死及其对自噬体融合物的裂解作用一致,导致潜伏性结核感染。因此,我们旨在全面分析结核分枝杆菌的自噬和自我防御机制,以期为未来针对结核病的新型治疗工具和诊断标志物的研究带来可喜的结果。

更新日期:2024-03-08
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