Src-family kinase dependent disruption of endothelial barrier function by Plasmodium falciparum merozoite proteins.

ABSTRACT: Pulmonary complication in severe Plasmodium falciparum malaria is manifested as a prolonged impairment of gas transfer or the more severe acute respiratory distress syndrome (ARDS). In either clinical presentation, vascular permeability is a major component of the pathologic process. In this report, we examined the effect of clinical P falciparum isolates on barrier function of primary dermal and lung microvascular endothelium in vitro. We showed that parasite sonicates but not intact infected erythrocytes disrupted endothelial barrier function in a Src-family kinase-dependent manner. The abnormalities were manifested both as discontinuous immunofluorescence staining of the junctional proteins ZO-1, claudin 5, and VE-cadherin and the formation of interendothelial gaps in monolayers. These

SUBMITTER: Gillrie MR 

PROVIDER: S-EPMC2200906 | biostudies-literature | 2007 Nov

REPOSITORIES: biostudies-literature