Authors
Leoratti, Fabiana Maria de SouzaTrevelin, Silvia Cellone
Cunha, Fernando Queiroz
Rocha, Bruno Coelho
Costa, Pedro Augusto Carvalho
Gravina, Humberto Doriguetto
Tada, Mauro Shugiro
Pereira, Dhelio Batista
Golenbock, Douglas T.
Antonelli, Lis Ribeiro do Valle
Gazzinelli, Ricardo T.
UMass Chan Affiliations
Department of Medicine, Division of Infectious Diseases and ImmunologyDocument Type
Journal ArticlePublication Date
2012-01-01Keywords
malarianeutrophils
Immunity
Immunology and Infectious Disease
Immunology of Infectious Disease
Infectious Disease
Parasitic Diseases
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Show full item recordAbstract
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.Source
PLoS Negl Trop Dis. 2012;6(6):e1710. doi: 10.1371/journal.pntd.0001710. Epub 2012 Jun 26. Link to article on publisher's site
DOI
10.1371/journal.pntd.0001710Permanent Link to this Item
http://hdl.handle.net/20.500.14038/35159PubMed ID
22745844Related Resources
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Copyright: © 2012 Leoratti et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.Distribution License
http://creativecommons.org/licenses/by/4.0/ae974a485f413a2113503eed53cd6c53
10.1371/journal.pntd.0001710
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Except where otherwise noted, this item's license is described as Copyright: © 2012 Leoratti et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.