Academic Journal
Mycobacterium tuberculosis hijacks host macrophages-derived interleukin 16 to block phagolysosome maturation for enhancing intracellular growth
| العنوان: | Mycobacterium tuberculosis hijacks host macrophages-derived interleukin 16 to block phagolysosome maturation for enhancing intracellular growth |
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| المؤلفون: | Haibo Su, Shufeng Weng, Liulin Luo, Qin Sun, Taiyue Lin, Huixia Ma, Yumo He, Jing Wu, Honghai Wang, Wenhong Zhang, Ying Xu |
| المصدر: | Emerging Microbes and Infections, Vol 13, Iss 1 (2024) |
| بيانات النشر: | Taylor & Francis Group, 2024. |
| سنة النشر: | 2024 |
| المجموعة: | LCC:Infectious and parasitic diseases LCC:Microbiology |
| مصطلحات موضوعية: | Mycobacterium tuberculosis, phagolysosome conversion, IL-16, macrophages, TB, Infectious and parasitic diseases, RC109-216, Microbiology, QR1-502 |
| الوصف: | The discovery of promising cytokines and clarification of their immunological mechanisms in controlling the intracellular fate of Mycobacterium tuberculosis (Mtb) are necessary to identify effective diagnostic biomarkers and therapeutic targets. To escape immune clearance, Mtb can manipulate and inhibit the normal host process of phagosome maturation. Phagosome maturation arrest by Mtb involves multiple effectors and much remains unknown about this important aspect of Mtb pathogenesis. In this study, we found that interleukin 16 (IL-16) is elevated in the serum samples of Tuberculosis (TB) patients and can serve as a specific target for treatment TB. There was a significant difference in IL-16 levels among active TB, latent TB infection (LTBI), and non-TB patients. This study first revealed that macrophages are the major source of IL-16 production in response to Mtb infection, and elucidated that IL-16 can promote Mtb intracellular survival by inhibiting phagosome maturation and suppressing the expression of Rev-erbα which can inhibit IL-10 secretion. The experiments using zebrafish larvae infected with M. marinum and mice challenged with H37Rv demonstrated that reducing IL-16 levels resulted in less severe pathology and improved survival, respectively. In conclusion, this study provided direct evidence that Mtb hijacks the host macrophages-derived interleukin 16 to enhance intracellular growth. It is suggesting the immunosuppressive role of IL-16 during Mtb infection, supporting IL-16 as a promising therapeutic target. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 22221751 2222-1751 |
| Relation: | https://doaj.org/toc/2222-1751 |
| DOI: | 10.1080/22221751.2024.2322663 |
| URL الوصول: | https://doaj.org/article/49cabce2b4c54256b5ec7940d0a36fea |
| رقم الانضمام: | edsdoj.49cabce2b4c54256b5ec7940d0a36fea |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 22221751 |
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| DOI: | 10.1080/22221751.2024.2322663 |