Acanthamoeba castellanii trophozoites escape killing by neutrophil extracellular traps using their 3'-nucleotidase/nuclease activity.

Autor: Carvalho-Kelly LF; Instituto de Bioquímica Médica Leopoldo de Meis (IBqM), UFRJ, Rio de Janeiro, RJ, Brazil. Electronic address: lfernandock@gmail.com., Freitas-Mesquita AL; Instituto de Bioquímica Médica Leopoldo de Meis (IBqM), UFRJ, Rio de Janeiro, RJ, Brazil., Nascimento MTC; Instituto de Bioquímica Médica Leopoldo de Meis (IBqM), UFRJ, Rio de Janeiro, RJ, Brazil; Instituto de Microbiologia Paulo de Góes (IMPG), UFRJ, Rio de Janeiro, RJ, Brazil., Dick CF; Instituto de Biofísica Carlos Chagas Filho (IBCCF), UFRJ, Rio de Janeiro, RJ, Brazil., de Souza-Maciel E; Instituto de Bioquímica Médica Leopoldo de Meis (IBqM), UFRJ, Rio de Janeiro, RJ, Brazil., Rochael NC; Instituto de Microbiologia Paulo de Góes (IMPG), UFRJ, Rio de Janeiro, RJ, Brazil., Saraiva EM; Instituto de Microbiologia Paulo de Góes (IMPG), UFRJ, Rio de Janeiro, RJ, Brazil., Meyer-Fernandes JR; Instituto de Bioquímica Médica Leopoldo de Meis (IBqM), UFRJ, Rio de Janeiro, RJ, Brazil.
Jazyk: angličtina
Zdroj: European journal of protistology [Eur J Protistol] 2023 Oct; Vol. 91, pp. 126032. Date of Electronic Publication: 2023 Oct 31.
DOI: 10.1016/j.ejop.2023.126032
Abstrakt: Acanthamoeba castellanii is a free-living amoeba that acts as an opportunistic pathogen for humans and is the pathogenic agent of Acanthamoeba keratitis (AK). A. castellanii may present as proliferative and infective trophozoites or as resistant cysts during their life cycle. The immune response against AK is still poorly explored; however, it is well established that macrophages and neutrophils play essential roles in controlling corneal infection during the disease outcome. The release of NETs is one of the innate immune strategies to prevent parasite infection, especially when neutrophils interact with microorganisms that are too large to be phagocytosed, which is the case for amoeba species. The present work demonstrated that A. castellanii trophozoites can trigger NET formation upon in vitro interaction with neutrophils. Using DNase as a control, we observed increased parasite survival after coinciding with neutrophils, which may be correlated with NET degradation. Indeed, A. castellanii trophozoites degrade the NET DNA scaffold. Molecular analysis confirmed the occurrence of a 3'-nucleotidase/nuclease (3'-NT/NU) in the A. castellanii genome. We also demonstrated that trophozoites exhibit significantly higher 3'-NT/NU activity than cysts, which cannot trigger NET release. Considering that previous studies indicated the pathological role of 3'-NT-/NU in parasite infection, we suggest that this enzyme may act as the mechanism of escape of A. castellanii trophozoites from NETs.
Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2023 Elsevier GmbH. All rights reserved.)
Databáze: MEDLINE
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