Neutrophil paralysis in Plasmodium vivax malaria.

BACKGROUND:The activation of innate immune responses by Plasmodium vivax results in activation of effector cells and an excessive production of pro-inflammatory cytokines that may culminate in deleterious effects. Here, we examined the activation and function of neutrophils during acute episodes of...

Full description

Bibliographic Details
Published in:PLoS Neglected Tropical Diseases
Main Authors: Fabiana Maria de Souza Leoratti, Silvia Cellone Trevelin, Fernando Queiroz Cunha, Bruno Coelho Rocha, Pedro Augusto Carvalho Costa, Humberto Doriguêtto Gravina, Mauro Shugiro Tada, Dhelio Batista Pereira, Douglas Taylor Golenbock, Lis Ribeiro do Valle Antonelli, Ricardo T Gazzinelli
Format: Article in Journal/Newspaper
Language:English
Published: Public Library of Science (PLoS) 2012
Subjects:
Arctic medicine. Tropical medicine
RC955-962
Public aspects of medicine
RA1-1270
Arctic
Online Access:https://doi.org/10.1371/journal.pntd.0001710
https://doaj.org/article/79837094175c4ecb9ae56910053fc299
Description
Summary:BACKGROUND:The activation of innate immune responses by Plasmodium vivax results in activation of effector cells and an excessive production of pro-inflammatory cytokines that may culminate in deleterious effects. Here, we examined the activation and function of neutrophils during acute episodes of malaria. MATERIALS AND METHODS:Blood samples were collected from P. vivax-infected patients at admission (day 0) and 30-45 days after treatment with chloroquine and primaquine. Expression of activation markers and cytokine levels produced by highly purified monocytes and neutrophils were measured by the Cytometric Bead Assay. Phagocytic activity, superoxide production, chemotaxis and the presence of G protein-coupled receptor (GRK2) were also evaluated in neutrophils from malaria patients. PRINCIPAL FINDINGS:Both monocytes and neutrophils from P. vivax-infected patients were highly activated. While monocytes were found to be the main source of cytokines in response to TLR ligands, neutrophils showed enhanced phagocytic activity and superoxide production. Interestingly, neutrophils from the malaria patients expressed high levels of GRK2, low levels of CXCR2, and displayed impaired chemotaxis towards IL-8 (CXCL8). CONCLUSION:Activated neutrophils from malaria patients are a poor source of pro-inflammatory cytokines and display reduced chemotactic activity, suggesting a possible mechanism for an enhanced susceptibility to secondary bacterial infection during malaria.

Similar Items