ArticleBMC pulmonary medicine2022
Extracellular vesicles from serum samples of mycobacteria patients induced cell death of THP-1 monocyte and PBMC.
Article in BMC pulmonary medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- Extracellular Vesicles of Mycobacterium tuberculosis Serve as a Virulence Factor - Current Research Applications.Current microbiology · 2026Review
- Impact of L-arginine and L-citrulline supplementation on macrophage responses toFrontiers in immunology · 2026Article
- Tuberculosis Patients' Serum Extracellular Vesicles Induce Relevant Immune Responses for Initial Defense Against BCG in Mice.Microorganisms · 2025Article
- Extracellular Vesicles and Their Role in Lung Infections.International journal of molecular sciences · 2023Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExtracellular vesicles (EVs) play a key role in cell communication and the pathogenesis of some diseases. EVs may accelerate cell death during the course of mycobacterial infection and are also considered as a new vaccine design, drug delivery, and biomarker candidates. The current study evaluates the effects of EVs from serum samples of mycobacteria-infected patients on THP-1 monocytes and PBMC cells.
methodEVs were purified from the serum, then cultured separately with THP-1 monocytes and PBMCs. The cell death was determined through annexin V-FITC and PI staining. GW4869, an EVs inhibitor, was used to determine if EVs released from serum could increase THP-1 monocytes cell death.
resultsThe cell death was significantly increased in the presence of 10 µg/ml and 5 µg/ml concentrations of the purified EVs (p < 0.05). Minimal cell death was determined in 2.5 µg/ml and 1.2 µg/ml (p < 0.05). Up to 85% of the cells were viable in the presence of the GW4869 inhibitor (p < 0.05).
conclusionDirect infection of the cells with EVs released from mycobacteria-infected patients samples, the multiplicity of infection with the EVs, and virulent or avirulent mycobacteria may change the status of the cell death. The isolated EVs from serum samples of patients with mycobacterial infection accelerated cell death, which means that they might not be considered as an optimal tool for developing drug delivery and vaccine against tuberculosis.
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