Increased iron stores correlate with worse disease outcomes in a mouse model of schistosomiasis infection

McDonald, Cameron J., Jones, Malcolm K., Wallace, Daniel F., Summerville, Lesa, Nawaratna, Sujeevi and Subramaniam, V. Nathan (2010) Increased iron stores correlate with worse disease outcomes in a mouse model of schistosomiasis infection. PLoS One, 5 3: 1-7. doi:10.1371/journal.pone.0009594


Author McDonald, Cameron J.
Jones, Malcolm K.
Wallace, Daniel F.
Summerville, Lesa
Nawaratna, Sujeevi
Subramaniam, V. Nathan
Title Increased iron stores correlate with worse disease outcomes in a mouse model of schistosomiasis infection
Journal name PLoS One   Check publisher's open access policy
ISSN 1932-6203
Publication date 2010-03
Sub-type Article (original research)
DOI 10.1371/journal.pone.0009594
Open Access Status DOI
Volume 5
Issue 3
Start page 1
End page 7
Total pages 7
Editor Peter Binfield
Place of publication San Francisco, CA, U.S.A.
Publisher Public Library of Science
Collection year 2011
Language eng
Formatted abstract
Schistosomiasis is a significant parasitic infection creating disease burden throughout many of the world's developing nations. Iron deficiency anemia is also a significant health burden resulting from both nutritional deficit as well as parasitic infection in these countries. In this study we investigated the relationships between the disease outcomes of Schistosoma japonicum infection and iron homeostasis. We aimed to determine if host iron status has an effect on schistosome maturation or egg production, and to investigate the response of iron regulatory genes to chronic schistosomiasis infection. Wild-type C57BL/6 and Transferrin Receptor 2 null mice were infected with S. japonicum, and sacrificed at the onset of chronic disease. Transferrin Receptor 2 null mice are a model of type 3 hereditary hemochromatosis and develop significant iron overload providing increased iron stores at the onset of infection. The infectivity of schistosomes and egg production was assessed along with the subsequent development of granulomas and fibrosis. The response of the iron regulatory gene Hepcidin to infection and the changes in iron status were assessed by real-time PCR and Western blotting. Our results show that Hepcidin levels responded to the changing iron status of the animals, but were not significantly influenced by the inflammatory response. We also show that with increased iron availability at the time of infection there was greater development of fibrosis around granulomas. In conclusion, our studies indicate that chronic inflammation may not be the primary cause of the anemia seen in schistosomiasis, and suggest that increased availability of iron, such as through iron supplementation, may actually lead to increased disease severity.
© 2010 McDonald et al.
Keyword Hepatic stellate cells
Helminth infections
Young adults
Anemia
Hepcidin
Japonicum
Hemochomatosis
Inflammation
Transferrin
Philippines
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2011 Collection
School of Medicine Publications
 
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Citation counts: TR Web of Science Citation Count  Cited 17 times in Thomson Reuters Web of Science Article | Citations
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Created: Sun, 21 Mar 2010, 00:01:03 EST