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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 changes were associated with a loss in total protein content of claudin 5 and redistribution of ZO-1 from the cytoskeleton to the membrane and the cytosolic and nuclear fractions. There was minimal evidence of a proinflammatory response or direct cellular cytotoxicity or cell death. The active component in sonicates appeared to be a merozoite-associated protein. Increased permeability was also induced by P falciparum glycophosphatidylinositols (GPIs) and food vacuoles. These results demonstrate that parasite components can alter endothelial barrier function and thus contribute to the pathogenesis of severe falciparum malaria.

journal_name

Blood

journal_title

Blood

authors

Gillrie MR,Krishnegowda G,Lee K,Buret AG,Robbins SM,Looareesuwan S,Gowda DC,Ho M

doi

10.1182/blood-2007-04-084582

subject

Has Abstract

pub_date

2007-11-01 00:00:00

pages

3426-35

issue

9

eissn

0006-4971

issn

1528-0020

pii

blood-2007-04-084582

journal_volume

110

pub_type

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