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Updated: Jun 13, 2025
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Identification of Virulence Markers of Mycobacterium abscessus for Intracellular Replication in Phagocytes
Published on: September 27, 2018
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Characterization of Exosomes Released from Mycobacterium abscessus-Infected Macrophages
Charlie A Vermeire1,2, Xuejuan Tan1,2, Aidaly Ramos-Leyva1,2
1Department of Biochemistry and Molecular Biology, Oklahoma State University, Stillwater, Oklahoma, USA.
Proteomics
|September 16, 2024
Summary
Mycobacterium abscessus infection prompts macrophages to release exosomes that deplete glutamine in recipient cells, hindering bacterial killing. Restoring glutamine levels rescues this effect, revealing a novel host-pathogen interaction mechanism.
Area of Science:
- Cell Biology
- Microbiology
- Immunology
Background:
- Extracellular vesicles (EVs), including exosomes, are key mediators of intercellular communication.
- Non-tuberculous mycobacteria (NTM), like Mycobacterium abscessus, cause severe lung infections, particularly in individuals with cystic fibrosis (CF) or chronic obstructive pulmonary disease (COPD).
- The role of EVs in host-pathogen interactions during NTM infections remains largely unexplored.
Purpose of the Study:
- To investigate the role of exosomes released by macrophages during Mycobacterium abscessus infection.
- To determine how these exosomes influence host-pathogen dynamics and bacterial growth.
- To elucidate the underlying molecular mechanisms, focusing on nutrient availability.
Main Methods:
- Macrophage cell cultures were infected with Mycobacterium abscessus.
- Exosomes released by infected and uninfected macrophages were isolated and characterized.
- Proteomic analysis was performed on isolated exosomes.
- The impact of exosomes on recipient macrophages and M. abscessus growth was assessed.
- Glutamine levels in recipient macrophages were measured and manipulated.
Main Results:
- Mycobacterium abscessus infection stimulated the release of specific exosome subpopulations (CD9, CD63, CD81 positive) from mouse macrophages.
- Proteomic analysis revealed altered host protein enrichment in exosomes from infected macrophages.
- Exosomes from M. abscessus-infected macrophages promoted bacterial growth and reduced intracellular glutamine levels in recipient macrophages.
- Supplementation of glutamine in the culture medium reversed the exosome-mediated effects, restoring glutamine levels and enhancing M. abscessus killing.
Conclusions:
- Exosomes released by M. abscessus-infected macrophages act as extracellular glutamine scavengers.
- This exosome-mediated glutamine depletion impairs the host's ability to kill M. abscessus within recipient macrophages.
- These findings uncover a novel mechanism by which NTM evades host immunity through exosome-mediated nutrient manipulation.
