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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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Published in: | Parasite immunology 2016-08, Vol.38 (8), p.481-495 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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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
. |
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ISSN: | 0141-9838 1365-3024 |
DOI: | 10.1111/pim.12337 |