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31 results on '"Cho, Soo-Na"'

12. Additional file 1 of Lipocalin 2 regulates expression of MHC class I molecules in Mycobacterium tuberculosis-infected dendritic cells via ROS production

Author

Choi, Ji-Ae, Cho, Soo-Na, Lee, Junghwan, Son, Sang-Hun, Nguyen, Doan Tam, Lee, Seong-Ahn, and Song, Chang-Hwa

Subjects
chemical and pharmacologic phenomena, respiratory system, bacterial infections and mycoses
Abstract

Additional file 1: Figure S1. LCN2 is induced following Mtb infection in BMDCs. Figure S2. LCN2 induced ROS-related molecules in Mtb-infected BMDCs. Figure S3. Effects of LCN2-mediated ROS on formation of the PLC in BMDCs. Figure S4. LCN2 regulates MHC class I molecule expression and CD8+ effector T-cell generation following intravenous Mtb infection. Figure S5. LCN2 does not affect the total T-cell population following Mtb infection. Figure S6. LCN2 in BMDCs is important to regulate CD8+ effector T-cell generation following Mtb infection. Figure S7. Mtb-induced effector CD8+ T cells regulate intracellular Mtb. Figure S8. LCN2 induced ROS-related molecules in Mtb-infected BMDCs. Figure S9. LCN2 regulates intracellular Mtb survival.

Published
2021
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24. Enhancement of the antimycobacterial activity of macrophages by ajoene.

Author

Choi, Ji-Ae, Cho, Soo-Na, Lim, Yun-Ji, Lee, Junghwan, Go, Dam, Kim, Seon-Hwa, and Song, Chang-Hwa

Subjects
*TUBERCULOSIS treatment, *MACROPHAGES, *ANTI-infective agents, *AJOENE, *ACTIVE oxygen in the body, *C-Jun N-terminal kinases
Abstract

Ajoene, a garlic-derived sulfur-containing compound, has broad-spectrum antimicrobial activity. To assess the potential of ajoene for treating tuberculosis (TB), we determined whether it induces the stress response of the endoplasmic reticulum (ER), which plays an important role in TB. We showed that ajoene stimulation induced the production of ER stress sensor molecules and reactive oxygen species (ROS) levels. Ajoene-induced ROS production was dependent on c-Jun N-terminal kinase (JNK) activation. Interestingly, the inhibition of JNK activity and suppression of ROS production reduced ajoene-induced CHOP production in macrophages. Because ER stress activates autophagy, the activation of which suppresses the growth of mycobacteria, we investigated the ajoene-induced production of autophagy-related factors, including LC3-II, P62 and Beclin-1. As expected, ajoene treatment increased the levels of these factors in RAW 264.7 cells. Remarkably, the total amount of Mycobacterium tuberculosis (Mtb) H37Rv was significantly reduced in ajoene-treated RAW 264.7 cells. The treatment of macrophages with ajoene resulted in the activation of JNK, induction of ROS synthesis and accumulation of ROS, possibly leading to the activation of ER stress and autophagy. These results reveal the mechanism of the antimycobacterial effects of ajoene against Mtb H37Rv. Our findings might facilitate the development of novel therapies for patients with TB. [ABSTRACT FROM AUTHOR]

Published
2018
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31. Reactive oxygen species‐mediated endoplasmic reticulum stress response induces apoptosis of Mycobacterium avium‐infected macrophages by activating regulated IRE1‐dependent decay pathway.

Author

Go, Dam, Lee, Junghwan, Choi, Ji‐Ae, Cho, Soo‐Na, Kim, Seon‐Hwa, Son, Sang‐Hun, and Song, Chang‐Hwa

Subjects
ENDOPLASMIC reticulum, REACTIVE oxygen species, MACROPHAGES, MYCOBACTERIUM, MYCOBACTERIUM avium, GENETIC regulation
Abstract

Mycobacterium avium, a slow‐growing nontuberculous mycobacterium, causes fever, diarrhoea, loss of appetite, and weight loss in immunocompromised people. We have proposed that endoplasmic reticulum (ER) stress‐mediated apoptosis plays a critical role in removing intracellular mycobacteria. In the present study, we investigated the role of the regulated IRE1‐dependent decay (RIDD) pathway in macrophages during M. avium infection based on its role in the regulation of gene expression. The inositol‐requiring enzyme 1 (IRE1)/apoptosis signal‐regulating kinase 1 (ASK1)/c‐Jun N‐terminal kinase (JNK) signalling pathway was activated in macrophages after infection with M. avium. The expression of RIDD‐associated genes, such as Bloc1s1 and St3gal5, was decreased in M. avium‐infected macrophages. Interestingly, M. avium‐induced apoptosis was significantly suppressed by pretreatment with irestatin (inhibitor of IRE1α) and 4μ8c (RIDD blocker). Macrophages pretreated with N‐acetyl cysteine (NAC) showed decreased levels of reactive oxygen species (ROS), IRE1α, and apoptosis after M. avium infection. The expression of Bloc1s1 and St3gal5 was increased in NAC‐pretreated macrophages following infection with M. avium. Growth of M. avium was significantly increased in irestatin‐, 4μ8c‐, and NAC‐treated macrophages compared with the control. The data indicate that the ROS‐mediated ER stress response induces apoptosis of M. avium‐infected macrophages by activating IRE1α‐RIDD. Thus, activation of IRE1α suppresses the intracellular survival of M. avium in macrophages. [ABSTRACT FROM AUTHOR]

Published
2019
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