Characterization of Endoplasmic Reticulum Stress and Apoptosis in Macrophages Infected with Mycobacterium tuberculosis Isolates from Korea Patients.
10.4167/jbv.2015.45.3.215
- Author:
Jung Hwan LEE
1
;
Yun Ji LIM
;
Ji Ae CHOI
;
Ji Ye HAN
;
Sung Hee CHO
;
Sung Man OH
;
Chang Hwa SONG
Author Information
1. Department of Microbiology, College of Medicine, Chungnam National University, Daejeon, Korea. songch@cnu.ac.kr
- Publication Type:Original Article
- Keywords:
Mycobacterium tuberculosis;
ER stress;
MCPIP
- MeSH:
Animals;
Apoptosis*;
Endoplasmic Reticulum Stress*;
Endoplasmic Reticulum*;
Humans;
Korea*;
Macrophages*;
Mice;
Mycobacterium tuberculosis*;
Mycobacterium*
- From:Journal of Bacteriology and Virology
2015;45(3):215-227
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Apoptosis is an important host defense mechanism against mycobacterial infection. Recent reports suggest that links between apoptosis and endoplasmic reticulum (ER) stress are critical for the regulation of mycobacterial survival; however, the exact regulatory mechanisms are not well known. In this study, we isolated 20 Mycobacterium tuberculosis (Mtb) clinical strains from Korean patients and examined ER stress-mediated apoptosis in Mtb-infected macrophages. Most Mtb strains increased the rates of apoptosis and production of ER stress-sensing molecules in mouse macrophages, similar to Mtb H37Rv infection. Moreover, the intracellular survival of Mtb clinical isolates in macrophages was similar to that of H37Rv. Our data suggest that infection with Mtb downregulated MCP-1 and MCPIP. The regulation of MCPIP may decrease ROS production, leading to a reduction in ER stress-mediated apoptosis.
