Linked Life Data

20816846

Source:http://linkedlifedata.com/resource/pubmed/id/20816846

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2010-12-20
pubmed:abstractText
Lung complications during malaria infection can range from coughs and impairments in gas transfer to the development of acute respiratory distress syndrome (ARDS). Infecting C57BL/6 mice with Plasmodium berghei K173 strain (PbK) resulted in pulmonary oedema, capillaries congested with leukocytes and infected red blood cells (iRBCs), and leukocyte infiltration into the lungs. This new model of malaria-associated lung pathology, without any accompanying cerebral complications, allows the investigation of mechanisms leading to the lung disease. The activity of the amiloride-sensitive epithelial sodium channel (ENaC) in alveolar epithelial cells is decreased by several respiratory tract pathogens and this is suggested to contribute to pulmonary oedema. We show that PbK, a pathogen that remains in the circulation, also decreased the activity and expression of ENaC, suggesting that infectious agents can have indirect effects on ENaC activity in lung epithelial cells. The reduced ENaC activity may contribute to the pulmonary oedema induced by PbK malaria.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1879-0135
pubmed:author
pubmed:copyrightInfo
Copyright © 2010. Published by Elsevier Ltd.
pubmed:issnType
Electronic
pubmed:volume
41
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
81-8
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Reduced activity of the epithelial sodium channel in malaria-induced pulmonary oedema in mice.
pubmed:affiliation
Discipline of Pathology, School of Medical Sciences and Bosch Institute, University of Sydney, NSW 2006, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't