Journal
JOURNAL OF IMMUNOLOGY RESEARCH
Volume 2019, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2019/3105817
Keywords
-
Categories
Funding
- Sao Paulo Research Foundation (Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP), Brazil)
- Coordination of Improvement of Higher Level Personnel
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
- National Council for Scientific and Technological Development (Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq), Brazil)
- CAPES
- FAPESP [2013/20718-3, 2017/00077-4, 2013/00981-1, 2016/07030-3, 2014/20451-0, 2017/05782-8]
- CAPES/PNPD
- CNPq [131431/2017-0, 162730/2014-4, 133890/2016-3, 455863/2014-8]
Ask authors/readers for more resources
The severity of Plasmodium falciparum malaria is associated with parasite cytoadherence, but there is limited knowledge about the effect of parasite cytoadherence in malaria-associated acute respiratory distress syndrome (ARDS). Our objective was to evaluate the cytoadherence of infected red blood cells (iRBCs) in a murine model of ARDS and to appraise a potential function of endothelial protein C receptor (EPCR) in ARDS pathogenesis. DBA/2 mice infected with P. berghei ANKA were classified as ARDS- or hyperparasitemia- (HP-) developing mice according to respiratory parameters and parasitemia. Lungs, blood, and bronchoalveolar lavage were collected for gene expression or protein analyses. Primary cultures of microvascular lung endothelial cells from DBA/2 mice were analyzed for iRBC interactions. Lungs from ARDS-developing mice showed evidence of iRBC accumulation along with an increase in EPCR and TNF concentrations. Furthermore, TNF increased iRBC adherence in vitro. Dexamethasone-treated infected mice showed low levels of TNF and EPCR mRNA expression and, finally, decreased vascular permeability, thus protecting mice from ARDS. In conclusion, we identified that increased iRBC cytoadherence in the lungs underlies malaria-associated ARDS in DBA/2-infected mice and that inflammation increased cytoadherence capacity, suggesting a participation of EPCR and a conceivable target for drug development.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available