MAB_0676c-induced enhanced IL-10 production inhibits the autophagic flux via the MTOR/RUBCN pathway
Mycobacterium abscessus subsp. abscessus (M.abs) is a nontuberculous mycobacterium that can infect human lung macrophages, which poses a public health concern. Understanding its mechanism is crucial for developing strategies to combat M.abs infections. M.abs survives within host cells by inhibiting...
Saved in:
| Main Authors: | , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Taylor & Francis Group
2025-12-01
|
| Series: | Virulence |
| Subjects: | |
| Online Access: | https://www.tandfonline.com/doi/10.1080/21505594.2025.2529493 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1849321023710691328 |
|---|---|
| author | Dong Ho Kim Kyungho Woo Ho-Sung Park Hye-Soo Park Hwa-Jung Kim Chul Hee Choi |
| author_facet | Dong Ho Kim Kyungho Woo Ho-Sung Park Hye-Soo Park Hwa-Jung Kim Chul Hee Choi |
| author_sort | Dong Ho Kim |
| collection | DOAJ |
| description | Mycobacterium abscessus subsp. abscessus (M.abs) is a nontuberculous mycobacterium that can infect human lung macrophages, which poses a public health concern. Understanding its mechanism is crucial for developing strategies to combat M.abs infections. M.abs survives within host cells by inhibiting autophagy, a defense mechanism used against intracellular pathogens; therefore, we investigated the mechanism underlying autophagy inhibition and human lung macrophage infection by M.abs. This study focuses on the M.abs UC22 strain, which exhibits stronger inhibition of autophagic flux compared to the M.abs ATCC 19,977 strain. Central to this study is MAB_0676c, a protein secreted by M.abs UC22, and its effects on autophagic flux and the innate immune response, particularly its role in enhancing IL-10 production, a known autophagy regulator. Experiments showed that MAB_0676c expression stabilizes autophagy-related proteins while reducing LC3-LAMP2 co-localization in macrophages, thereby inhibiting autophagy and promoting bacterial growth. Furthermore, blocking IL-10 reduced both autophagy-related protein levels and the intracellular growth of MAB_0676c-expressing bacteria. Therefore, M.abs UC22 mediates intracellular survival by inhibiting autophagy through IL-10 production. Our study reveals bacterial immune-evasion tactics and identifies a potential therapeutic target for treating infectious diseases caused by nontuberculous mycobacteria. |
| format | Article |
| id | doaj-art-a6772f0d7cf44fd78051007123b3202b |
| institution | Kabale University |
| issn | 2150-5594 2150-5608 |
| language | English |
| publishDate | 2025-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Virulence |
| spelling | doaj-art-a6772f0d7cf44fd78051007123b3202b2025-08-20T03:49:54ZengTaylor & Francis GroupVirulence2150-55942150-56082025-12-0116110.1080/21505594.2025.2529493MAB_0676c-induced enhanced IL-10 production inhibits the autophagic flux via the MTOR/RUBCN pathwayDong Ho Kim0Kyungho Woo1Ho-Sung Park2Hye-Soo Park3Hwa-Jung Kim4Chul Hee Choi5Department of Microbiology, School of Medicine, Chungnam National University, Daejeon, South KoreaDepartment of Microbiology, School of Medicine, Chungnam National University, Daejeon, South KoreaDepartment of Microbiology, School of Medicine, Chungnam National University, Daejeon, South KoreaDepartment of Microbiology, School of Medicine, Chungnam National University, Daejeon, South KoreaDepartment of Microbiology, School of Medicine, Chungnam National University, Daejeon, South KoreaDepartment of Microbiology, School of Medicine, Chungnam National University, Daejeon, South KoreaMycobacterium abscessus subsp. abscessus (M.abs) is a nontuberculous mycobacterium that can infect human lung macrophages, which poses a public health concern. Understanding its mechanism is crucial for developing strategies to combat M.abs infections. M.abs survives within host cells by inhibiting autophagy, a defense mechanism used against intracellular pathogens; therefore, we investigated the mechanism underlying autophagy inhibition and human lung macrophage infection by M.abs. This study focuses on the M.abs UC22 strain, which exhibits stronger inhibition of autophagic flux compared to the M.abs ATCC 19,977 strain. Central to this study is MAB_0676c, a protein secreted by M.abs UC22, and its effects on autophagic flux and the innate immune response, particularly its role in enhancing IL-10 production, a known autophagy regulator. Experiments showed that MAB_0676c expression stabilizes autophagy-related proteins while reducing LC3-LAMP2 co-localization in macrophages, thereby inhibiting autophagy and promoting bacterial growth. Furthermore, blocking IL-10 reduced both autophagy-related protein levels and the intracellular growth of MAB_0676c-expressing bacteria. Therefore, M.abs UC22 mediates intracellular survival by inhibiting autophagy through IL-10 production. Our study reveals bacterial immune-evasion tactics and identifies a potential therapeutic target for treating infectious diseases caused by nontuberculous mycobacteria.https://www.tandfonline.com/doi/10.1080/21505594.2025.2529493AutophagyIL-10macrophageMycobacterium abscessus subsp. abscessusRUBCN |
| spellingShingle | Dong Ho Kim Kyungho Woo Ho-Sung Park Hye-Soo Park Hwa-Jung Kim Chul Hee Choi MAB_0676c-induced enhanced IL-10 production inhibits the autophagic flux via the MTOR/RUBCN pathway Virulence Autophagy IL-10 macrophage Mycobacterium abscessus subsp. abscessus RUBCN |
| title | MAB_0676c-induced enhanced IL-10 production inhibits the autophagic flux via the MTOR/RUBCN pathway |
| title_full | MAB_0676c-induced enhanced IL-10 production inhibits the autophagic flux via the MTOR/RUBCN pathway |
| title_fullStr | MAB_0676c-induced enhanced IL-10 production inhibits the autophagic flux via the MTOR/RUBCN pathway |
| title_full_unstemmed | MAB_0676c-induced enhanced IL-10 production inhibits the autophagic flux via the MTOR/RUBCN pathway |
| title_short | MAB_0676c-induced enhanced IL-10 production inhibits the autophagic flux via the MTOR/RUBCN pathway |
| title_sort | mab 0676c induced enhanced il 10 production inhibits the autophagic flux via the mtor rubcn pathway |
| topic | Autophagy IL-10 macrophage Mycobacterium abscessus subsp. abscessus RUBCN |
| url | https://www.tandfonline.com/doi/10.1080/21505594.2025.2529493 |
| work_keys_str_mv | AT donghokim mab0676cinducedenhancedil10productioninhibitstheautophagicfluxviathemtorrubcnpathway AT kyunghowoo mab0676cinducedenhancedil10productioninhibitstheautophagicfluxviathemtorrubcnpathway AT hosungpark mab0676cinducedenhancedil10productioninhibitstheautophagicfluxviathemtorrubcnpathway AT hyesoopark mab0676cinducedenhancedil10productioninhibitstheautophagicfluxviathemtorrubcnpathway AT hwajungkim mab0676cinducedenhancedil10productioninhibitstheautophagicfluxviathemtorrubcnpathway AT chulheechoi mab0676cinducedenhancedil10productioninhibitstheautophagicfluxviathemtorrubcnpathway |