Extracellular Vesicles from Naegleria fowleri Induce IL-8 Response in THP-1 Macrophage
Issued Date
2022-06-01
Resource Type
eISSN
20760817
Scopus ID
2-s2.0-85131696264
Journal Title
Pathogens
Volume
11
Issue
6
Rights Holder(s)
SCOPUS
Bibliographic Citation
Pathogens Vol.11 No.6 (2022)
Suggested Citation
Lertjuthaporn S., Somkird J., Lekmanee K., Atipimonpat A., Sukapirom K., Sawasdipokin H., Tiewcharoen S., Pattanapanyasat K., Khowawisetsut L. Extracellular Vesicles from Naegleria fowleri Induce IL-8 Response in THP-1 Macrophage. Pathogens Vol.11 No.6 (2022). doi:10.3390/pathogens11060632 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/84979
Title
Extracellular Vesicles from Naegleria fowleri Induce IL-8 Response in THP-1 Macrophage
Author's Affiliation
Other Contributor(s)
Abstract
Extracellular vesicles (EVs) released from pathogenic protozoans play crucial roles in host–parasite communication and disease pathogenesis. Naegleria fowleri is a free-living protozoan causing primary amoebic meningoencephalitis, a fatal disease in the central nervous system. This study aims to explore the roles of N. fowleri-derived EVs (Nf-EVs) in host–pathogen interactions using the THP-1 cell line as a model. The Nf-EVs were isolated from the N. fowleri trophozoite culture supernatant using sequential centrifugation and characterized by nanoparticle tracking analysis and transmission electron microscopy. The functional roles of Nf-EVs in the apoptosis and immune response induction of THP-1 monocytes and macrophages were examined by flow cytometry, quantitative PCR, and ELISA. Results showed that Nf-EVs displayed vesicles with bilayer membrane structure approximately 130–170 nm in diameter. The Nf-EVs can be internalized by macrophages and induce macrophage responses by induction of the expression of costimulatory molecules CD80, CD86, HLA-DR, and CD169 and the production of cytokine IL-8. However, Nf-EVs did not affect the apoptosis of macrophages. These findings illustrate the potential role of Nf-EVs in mediating the host immune cell activation and disease pathogenesis.