Skip to content
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Menu
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Menu
Home
About Us
Resources
Profiles Metrics
Authors Directory
Institutions Directory
Top Authors
Top Institutions
Top Sponsors
AI Digest
Contact Us
Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
biochemistry, genetics and molecular biology
Plasmodium falciparum Malaria Elicits Inflammatory Responses that Dysregulate Placental Amino Acid Transport
PLoS Pathogens, Volume 9, No. 2, Article e1003153, Year 2013
Notification
URL copied to clipboard!
Description
Placental malaria (PM) can lead to poor neonatal outcomes, including low birthweight due to fetal growth restriction (FGR), especially when associated with local inflammation (intervillositis or IV). The pathogenesis of PM-associated FGR is largely unknown, but in idiopathic FGR, impaired transplacental amino acid transport, especially through the system A group of amino acid transporters, has been implicated. We hypothesized that PM-associated FGR could result from impairment of transplacental amino acid transport triggered by IV. In a cohort of Malawian women and their infants, the expression and activity of system A (measured by Na+-dependent 14C-MeAIB uptake) were reduced in PM, especially when associated with IV, compared to uninfected placentas. In an in vitro model of PM with IV, placental cells exposed to monocyte/infected erythrocytes conditioned medium showed decreased system A activity. Amino acid concentrations analyzed by reversed phase ultra performance liquid chromatography in paired maternal and cord plasmas revealed specific alterations of amino acid transport by PM, especially with IV. Overall, our data suggest that the fetoplacental unit responds to PM by altering its placental amino acid transport to maintain adequate fetal growth. However, IV more profoundly compromises placental amino acid transport function, leading to FGR. Our study offers the first pathogenetic explanation for FGR in PM. © 2013 Boeuf et al.
Authors & Co-Authors
Boeuf, Philippe S.
Australia, Melbourne
University of Melbourne
Australia, Melbourne
Royal Melbourne Hospital
Aitken, Elizabeth Helen
Australia, Melbourne
University of Melbourne
Chandrasiri, Upeksha P.
Australia, Melbourne
University of Melbourne
Chua, Caroline Lin
Australia, Melbourne
University of Melbourne
McInerney, Bernie V.
Australia, Sydney
Macquarie University
McQuade, Leon R.
Australia, Sydney
Macquarie University
Duffy, Michael F.
Australia, Melbourne
University of Melbourne
Australia, Melbourne
Royal Melbourne Hospital
Molyneux, Malcolm Edward
Malawi, Zomba
University of Malawi
United Kingdom, Liverpool
Liverpool School of Tropical Medicine
Brown, Graham V.
Australia, Melbourne
University of Melbourne
Glazier, Jocelyn D.
United Kingdom, Manchester
The University of Manchester
Rogerson, Stephen J.
Australia, Melbourne
University of Melbourne
Australia, Melbourne
Royal Melbourne Hospital
Statistics
Citations: 78
Authors: 11
Affiliations: 6
Identifiers
Doi:
10.1371/journal.ppat.1003153
ISSN:
15537366
e-ISSN:
15537374
Research Areas
Infectious Diseases
Maternal And Child Health
Study Design
Cohort Study
Participants Gender
Female