Reduced activity of the epithelial sodium channel in malaria-induced pulmonary oedema in mice.
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.
Hee
Leia
L
Discipline of Pathology, School of Medical Sciences and Bosch Institute, University of Sydney, NSW 2006, Australia.
Dinudom
Anuwat
A
Mitchell
Andrew J
AJ
Grau
Georges E
GE
Cook
David I
DI
Hunt
Nicholas H
NH
Ball
Helen J
HJ
D000818:Animals; D053503:Epithelial Sodium Channels / Q000378:metabolism*; D005260:Female; D006651:Histocytochemistry; D007150:Immunohistochemistry; D008288:Malaria / Q000469:parasitology / Q000473:pathology / Q000662:veterinary*; D051379:Mice; D008810:Mice, Inbred C57BL; D008853:Microscopy; D010962:Plasmodium berghei / Q000472:pathogenicity*; D011650:Pulmonary Alveoli / Q000469:parasitology / Q000473:pathology*; D011654:Pulmonary Edema / Q000469:parasitology / Q000473:pathology / Q000662:veterinary*
D053503:Epithelial Sodium Channels
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