Contributions
Abstract: EP848
Type: E-Poster Presentation
Session title: Iron metabolism, deficiency and overload
Background
Severe malarial anemia (SMA) is a disease developed in the course of Plasmodium infection, which is often associated with increased rates of malaria-related morbidity and mortality. Despite high levels of erythropoietin (EPO), the occurrence of ineffective erythropoiesis is one of the main features of SMA. To gain new insights into the pathogenesis of malaria infection, changes in erythropoiesis associated with single or multiple infections with Plasmodium chabaudi chabaudi were investigated as well as the contribution of the immune system to the development of SMA.
Aims
Previous studies demonstrated that during anemia, proinflammatory cytokines suppress erythropoiesis by promoting iron sequestration through the hepatic hepcidin production. We confirmed that a similar response is presented in our SMA model by analyzing immune activation and the expression of iron metabolism associated genes. These data also showed that iron sensors expression levels, such as transferrin receptor 2 (Tfr2) and the hemochromatosis gene (HFE), are strictly associated with the disease severity. The extent of an immune response activation upon the exposure to this parasitic infection was also linked to the degree of induced SMA, with T cells playing a major role.
Methods
Flow cytometry analyses were used to show the bone marrow and spleen response during the infection.
Results
The results obtained demonstrated that malaria infection significantly alters the erythropoietic process through the dynamic interaction between inflammation and iron metabolism.
In order to regulate the erythropoietic response in malaria, the spleen increases erythrocyte production and compensate the loss of an appropriate bone marrow erythropoiesis during the infection. This directly correlates with parasite load.
Conclusion
In conclusion, malaria infection significantly alters the erythropoietic process through the dynamic interaction between inflammation and iron metabolism.
Keyword(s):
Abstract: EP848
Type: E-Poster Presentation
Session title: Iron metabolism, deficiency and overload
Background
Severe malarial anemia (SMA) is a disease developed in the course of Plasmodium infection, which is often associated with increased rates of malaria-related morbidity and mortality. Despite high levels of erythropoietin (EPO), the occurrence of ineffective erythropoiesis is one of the main features of SMA. To gain new insights into the pathogenesis of malaria infection, changes in erythropoiesis associated with single or multiple infections with Plasmodium chabaudi chabaudi were investigated as well as the contribution of the immune system to the development of SMA.
Aims
Previous studies demonstrated that during anemia, proinflammatory cytokines suppress erythropoiesis by promoting iron sequestration through the hepatic hepcidin production. We confirmed that a similar response is presented in our SMA model by analyzing immune activation and the expression of iron metabolism associated genes. These data also showed that iron sensors expression levels, such as transferrin receptor 2 (Tfr2) and the hemochromatosis gene (HFE), are strictly associated with the disease severity. The extent of an immune response activation upon the exposure to this parasitic infection was also linked to the degree of induced SMA, with T cells playing a major role.
Methods
Flow cytometry analyses were used to show the bone marrow and spleen response during the infection.
Results
The results obtained demonstrated that malaria infection significantly alters the erythropoietic process through the dynamic interaction between inflammation and iron metabolism.
In order to regulate the erythropoietic response in malaria, the spleen increases erythrocyte production and compensate the loss of an appropriate bone marrow erythropoiesis during the infection. This directly correlates with parasite load.
Conclusion
In conclusion, malaria infection significantly alters the erythropoietic process through the dynamic interaction between inflammation and iron metabolism.
Keyword(s):