PUBLICATION

Mycobacterium tuberculosis hijacks host macrophages-derived interleukin 16 to block phagolysosome maturation for enhancing intracellular growth

Authors
Su, H., Weng, S., Luo, L., Sun, Q., Lin, T., Ma, H., He, Y., Wu, J., Wang, H., Zhang, W., Xu, Y.
ID
ZDB-PUB-240222-13
Date
2024
Source
Emerging microbes & infections   13(1): 2322663 (Journal)
Registered Authors
Keywords
Mycobacterium tuberculosis, phagolysosome conversion, IL-16, macrophages, TB
MeSH Terms
  • Animals
  • Humans
  • Interleukin-16/metabolism
  • Macrophages/microbiology
  • Mice
  • Mycobacterium tuberculosis*
  • Phagosomes/metabolism
  • Phagosomes/microbiology
  • Tuberculosis*/microbiology
  • Zebrafish
(all 10)
PubMed
38380651 Full text @ Emerg Microbes Infect
Abstract
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.
Genes / Markers
Figures
Figure Gallery (8 images)
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Target Reagent Reagent Type
il16MO1-il16MRPHLNO
1 - 1 of 1
Show
Fish
Antibodies
Orthology
Engineered Foreign Genes
No data available
Mapping
Your Input Welcome
We welcome your input and comments. Please use this form to recommend updates to the information in ZFIN. We appreciate as much detail as possible and references as appropriate. We will review your comments promptly.
Citation
Su, H., Weng, S., Luo, L., Sun, Q., Lin, T., Ma, H., He, Y., Wu, J., Wang, H., Zhang, W., Xu, Y. (2024) Mycobacterium tuberculosis hijacks host macrophages-derived interleukin 16 to block phagolysosome maturation for enhancing intracellular growth. Emerging microbes & infections. 13(1):2322663.