Shrestha Dutta, Amity University Kolkata
Tuberculosis (TB), is one of the main causes of death around the world especially in children, is brought about by the infection of Mycobacterium tuberculosis (MTB). MTB infects the cell, stimulates immune response and triggers inflammation. Recent studies show that host-pathogen interaction is vital for TB pathogenesis and progression. MTB attacks macrophage of the host through different intercellular organelles to participate in different biological processes, for example, cell energy metabolism, inflammatory reaction, and endocytosis.
Mitochondria has a crucial role in the initiation and stimulation of the nucleotide-restricting oligomerization area like receptor with a pyrin domain 3 (NLRP3) inflammasome, where mitochondria-associated endoplasmic reticulum membranes (MAMs) may help in inflammasome aggregation and stimulation. Moreover, mitofusin 2 (MFN2) is involved in the formation of MAMs, yet, the functions of mitochondria and MFN2 in MTB disease have not been explained. Utilizing microarray profiling of TB patients and in vitro MTB activation of macrophages, we noticed an upregulation of MFN2 in the peripheral blood mononuclear cells of dynamic TB patients. Additionally, it was noticed that MTB activation by MTB-explicit antigen ESAT-6 or lysate of MTB promoted MFN2 interaction with NLRP3 inflammasomes, resulting in the aggregation and stimulation of the inflammasome and, therefore, IL-1β secretion. These discoveries propose that MFN2 and mitochondria assume a significant role in pathogen-host interaction during MTB contamination.
Also read: Evaluation of Functionality in Ni@stabilized ZrO2 and NiO@NiO-Zn through X-ray Diffraction Technique
Source:
http://m.jbc.org/content/early/2020/10/16/jbc.RA120.014077.short
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