Szczegóły publikacji
Opis bibliograficzny
Oxidative insult can induce malaria-protective trait of sickle and fetal erythrocytes / Marek Cyrklaff, [et al.], Kvetoslava BURDA, [et al.] // Nature Communications [Dokument elektroniczny]. — Czasopismo elektroniczne ; ISSN 2041-1723. — 2016 — vol. 7 art. no. 13401, s. 1–11. — Wymagania systemowe: Adobe Reader. — Bibliogr. s. 9–11. — Publikacja dostępna online od: 2016-11-08
Autorzy (13)
- Cyrklaff Marek
- AGHBurda Kvetoslava
Dane bibliometryczne
| ID BaDAP | 102718 |
|---|---|
| Data dodania do BaDAP | 2017-01-12 |
| Tekst źródłowy | URL |
| DOI | 10.1038/ncomms13401 |
| Rok publikacji | 2016 |
| Typ publikacji | artykuł w czasopiśmie |
| Otwarty dostęp |  |
| Creative Commons | |
| Czasopismo/seria | Nature Communications |
Abstract
Plasmodium falciparum infections can cause severe malaria, but not every infected person develops life-threatening complications. In particular, carriers of the structural haemoglobinopathies S and C and infants are protected from severe disease. Protection is associated with impaired parasite-induced host actin reorganization, required for vesicular trafficking of parasite-encoded adhesins, and reduced cytoadherence of parasitized erythrocytes in the microvasculature. Here we show that aberrant host actin remodelling and the ensuing reduced cytoadherence result from a redox imbalance inherent to haemoglobinopathic and fetal erythrocytes. We further show that a transient oxidative insult to wild-type erythrocytes before infection with P. falciparum induces the phenotypic features associated with the protective trait of haemoglobinopathic and fetal erythrocytes. Moreover, pretreatment of mice with the pro-oxidative nutritional supplement menadione mitigate the development of experimental cerebral malaria. Our results identify redox imbalance as a causative principle of protection from severe malaria, which might inspire host-directed intervention strategies.
