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Microvesicles Derived from Human Bronchial Epithelial Cells Regulate Macrophage Activation During Mycobacterium
Carlyn M Guthrie1,2, Amber C Meeker1,2, Ashton E Self1,2
1Department of Biochemistry and Molecular Biology, Oklahoma State University, Stillwater, Oklahoma 74078, United States.
Journal of Proteome Research
|March 28, 2025
Summary
Human airway cells release microvesicles upon Nontuberculous mycobacterium (NTM) infection. These microvesicles activate M2 macrophages, influencing host immunity and bacterial survival.
Area of Science:
- Immunology
- Cell Biology
- Microbiology
Background:
- Intercellular communication is crucial for host immunity against bacterial infections.
- Nontuberculous mycobacteria (NTM), like Mycobacterium abscessus (M. ab), cause severe lung infections, particularly in cystic fibrosis (CF) and COPD patients.
- Understanding host-pathogen interactions at the cellular level during NTM infection is limited.
Purpose of the Study:
- To characterize microvesicles (MVs) released by M. ab-infected human bronchial epithelial cells.
- To investigate the impact of these MVs on macrophage activation and polarization.
- To elucidate the role of MVs in host immune response to M. ab infection.
Main Methods:
- Isolation and characterization of microvesicles from M. ab-infected and uninfected human bronchial epithelial cells.
- Assessment of MV effects on THP-1-derived macrophage activation and polarization in cell culture.
- Proteomic analysis of isolated MVs to identify enriched proteins and pathways.
Main Results:
- MVs from M. ab-infected cells promoted M2 macrophage activation compared to MVs from uninfected cells.
- Proteomic analysis revealed enrichment of cell adhesion pathway proteins in MVs from infected cells.
- Intercellular adhesion molecule 1 (ICAM-1) on MVs regulated their uptake by macrophages.
Conclusions:
- Human airway epithelial cells release MVs in response to M. ab infection.
- These MVs modulate macrophage activation, influencing the host's immune response.
- The findings suggest a novel mechanism by which airway epithelial cells communicate with immune cells during NTM infections.
Keywords:
Mycobacterium abscessusepithelial cellsextracellular vesiclesintercellular communicationmacrophagesmicrovesiclesproteomicsMore Related Videos
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