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Neutrophils extracellular traps damage N aegleria fowleri trophozoites opsonized with human I g G

Naegleria fowleri infects humans through the nasal mucosa causing a disease in the central nervous system known as primary amoebic meningoencephalitis ( PAM ). Polymorphonuclear cells ( PMN s) play a critical role in the early phase of N. fowleri infection. Recently, a new biological defence mechani...

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Bibliographic Details
Published in:Parasite immunology 2016-08, Vol.38 (8), p.481-495
Main Authors: Contis‐Montes de Oca, A., Carrasco‐Yépez, M., Campos‐Rodríguez, R., Pacheco‐Yépez, J., Bonilla‐Lemus, P., Pérez‐López, J., Rojas‐Hernández, S.
Format: Article
Language:English
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Summary:Naegleria fowleri infects humans through the nasal mucosa causing a disease in the central nervous system known as primary amoebic meningoencephalitis ( PAM ). Polymorphonuclear cells ( PMN s) play a critical role in the early phase of N. fowleri infection. Recently, a new biological defence mechanism called neutrophil extracellular traps ( NET s) has been attracting attention. NET s are composed of nuclear DNA combined with histones and antibacterial proteins, and these structures are released from the cell to direct its antimicrobial attack. In this work, we evaluate the capacity of N. fowleri to induce the liberation of NET s by human PMN cells. Neutrophils were cocultured with unopsonized or IgG‐opsonized N. fowleri trophozoites. DNA , histone, myeloperoxidase ( MPO ) and neutrophil elastase ( NE ) were stained, and the formation of NET s was evaluated by confocal microscopy and by quantifying the levels of extracellular DNA . Our results showed N. fowleri induce the liberation of NET s including release of MPO and NE by human PMN cells as exposure interaction time is increased, but N. fowleri trophozoites evaded killing. However, when trophozoites were opsonized, they were susceptible to the neutrophils activity. Therefore, our study suggests that antibody‐mediated PMN s activation through NET formation may be crucial for antimicrobial responses against N. fowleri .
ISSN:0141-9838
1365-3024
DOI:10.1111/pim.12337