The WHY the low iron diet works for those with parasitical infection ..
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Increased Iron Stores Correlate with Worse Disease Outcomes in a Mouse Model of Schistosomiasis Infection Cameron J. McDonald1, Malcolm K. Jones2,3, Daniel F. Wallace1, Lesa Summerville1, Sujeevi Nawaratna2,3, V. Nathan Subramaniam1,4* 1 Membrane Transport Laboratory, Division of Cancer and Cell Biology, Queensland Institute of Medical Research, Brisbane, Queensland, Australia, 2 Parasite Cell Biology Laboratory, Division of Infectious Diseases and Immunology, Queensland Institute of Medical Research, Brisbane, Queensland, Australia, 3 School of Veterinary Science, The University of Queensland, Brisbane, Queensland, Australia, 4 Liver Research Centre, School of Medicine, The University of Queensland, Brisbane, Queensland, Australia
Abstract Top 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.
Citation: McDonald CJ, Jones MK, Wallace DF, Summerville L, Nawaratna S, et al. (2010) Increased Iron Stores Correlate with Worse Disease Outcomes in a Mouse Model of Schistosomiasis Infection. PLoS ONE 5(3): e9594. doi:10.1371/journal.pone.0009594
Editor: Ben L. Kelly, Louisiana State University, United States of America
Received: November 12, 2009; Accepted: February 15, 2010; Published: March 9, 2010
Funding: This work was supported in part by a Program Grant from the National Health and Medical Research Council (NHMRC) of Australia (339400) to VNS. DFW is the recipient of an NHMRC R. D. Wright Career Development Award. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
The WHY the low iron diet works for those with parasitical infection ..
-----------
Increased Iron Stores Correlate with Worse Disease Outcomes in a Mouse Model of Schistosomiasis Infection Cameron J. McDonald1, Malcolm K. Jones2,3, Daniel F. Wallace1, Lesa Summerville1, Sujeevi Nawaratna2,3, V. Nathan Subramaniam1,4* 1 Membrane Transport Laboratory, Division of Cancer and Cell Biology, Queensland Institute of Medical Research, Brisbane, Queensland, Australia, 2 Parasite Cell Biology Laboratory, Division of Infectious Diseases and Immunology, Queensland Institute of Medical Research, Brisbane, Queensland, Australia, 3 School of Veterinary Science, The University of Queensland, Brisbane, Queensland, Australia, 4 Liver Research Centre, School of Medicine, The University of Queensland, Brisbane, Queensland, Australia
Abstract Top 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.
Citation: McDonald CJ, Jones MK, Wallace DF, Summerville L, Nawaratna S, et al. (2010) Increased Iron Stores Correlate with Worse Disease Outcomes in a Mouse Model of Schistosomiasis Infection. PLoS ONE 5(3): e9594. doi:10.1371/journal.pone.0009594
Editor: Ben L. Kelly, Louisiana State University, United States of America
Received: November 12, 2009; Accepted: February 15, 2010; Published: March 9, 2010
Funding: This work was supported in part by a Program Grant from the National Health and Medical Research Council (NHMRC) of Australia (339400) to VNS. DFW is the recipient of an NHMRC R. D. Wright Career Development Award. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
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The WHY the low iron diet works for those with parasitical infection ..
-----------
Increased Iron Stores Correlate with Worse Disease Outcomes in a Mouse Model of Schistosomiasis Infection Cameron J. McDonald1, Malcolm K. Jones2,3, Daniel F. Wallace1, Lesa Summerville1, Sujeevi Nawaratna2,3, V. Nathan Subramaniam1,4* 1 Membrane Transport Laboratory, Division of Cancer and Cell Biology, Queensland Institute of Medical Research, Brisbane, Queensland, Australia, 2 Parasite Cell Biology Laboratory, Division of Infectious Diseases and Immunology, Queensland Institute of Medical Research, Brisbane, Queensland, Australia, 3 School of Veterinary Science, The University of Queensland, Brisbane, Queensland, Australia, 4 Liver Research Centre, School of Medicine, The University of Queensland, Brisbane, Queensland, Australia
Abstract Top 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.
Citation: McDonald CJ, Jones MK, Wallace DF, Summerville L, Nawaratna S, et al. (2010) Increased Iron Stores Correlate with Worse Disease Outcomes in a Mouse Model of Schistosomiasis Infection. PLoS ONE 5(3): e9594. doi:10.1371/journal.pone.0009594
Editor: Ben L. Kelly, Louisiana State University, United States of America
Received: November 12, 2009; Accepted: February 15, 2010; Published: March 9, 2010
Funding: This work was supported in part by a Program Grant from the National Health and Medical Research Council (NHMRC) of Australia (339400) to VNS. DFW is the recipient of an NHMRC R. D. Wright Career Development Award. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
An American atheist same-sex sexual predator is trying to disrupt this thread .. ignore him ...
The WHY the low iron diet works for those with parasitical infection ..
-----------
Increased Iron Stores Correlate with Worse Disease Outcomes in a Mouse Model of Schistosomiasis Infection Cameron J. McDonald1, Malcolm K. Jones2,3, Daniel F. Wallace1, Lesa Summerville1, Sujeevi Nawaratna2,3, V. Nathan Subramaniam1,4* 1 Membrane Transport Laboratory, Division of Cancer and Cell Biology, Queensland Institute of Medical Research, Brisbane, Queensland, Australia, 2 Parasite Cell Biology Laboratory, Division of Infectious Diseases and Immunology, Queensland Institute of Medical Research, Brisbane, Queensland, Australia, 3 School of Veterinary Science, The University of Queensland, Brisbane, Queensland, Australia, 4 Liver Research Centre, School of Medicine, The University of Queensland, Brisbane, Queensland, Australia
Abstract Top 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.
Citation: McDonald CJ, Jones MK, Wallace DF, Summerville L, Nawaratna S, et al. (2010) Increased Iron Stores Correlate with Worse Disease Outcomes in a Mouse Model of Schistosomiasis Infection. PLoS ONE 5(3): e9594. doi:10.1371/journal.pone.0009594
Editor: Ben L. Kelly, Louisiana State University, United States of America
Received: November 12, 2009; Accepted: February 15, 2010; Published: March 9, 2010
Funding: This work was supported in part by a Program Grant from the National Health and Medical Research Council (NHMRC) of Australia (339400) to VNS. DFW is the recipient of an NHMRC R. D. Wright Career Development Award. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
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