Carla Cerami, PhD
|1993||New York University School of Medicine||MD, Medicine|
|1993||New York University School of Medicine||PhD, Immunology|
|1987||Columbia College||BA, Biochemistry|
- Global health
- Infectious diseases
My focus is on two areas of global health research (1) iron at the interface of the host pathogen interaction and (2) trauma.
Iron at the interface of the host pathogen interaction: Our goal is to shed light on the biological principles governing clinical observations that iron deficiency is protective against malaria infection and that iron supplementation increases an individual’s risk of malaria and bacterial infections. It had been previously hypothesized that iron deficiency inhibited malaria growth through iron deprivation, as is the case with other pathogens, however, our work, has shown that the effects of iron deficiency and iron supplementation on parasite growth are due to changes in red blood cell physiology and the age structure of the red blood cell population. We have shown that the malaria parasite has decreased invasion into and growth within red blood cells from subjects with iron deficiency. Additionally, we have shown that red blood cells from subjects who respond to iron supplementation with an increased erythropoietic rate demonstrate increased susceptibility to P. falciparum infection. These novel findings have public health implications on the wisdom of providing malaria prophylaxis during iron supplementation and may serve as a pathway to better understand the relationship between the parasite and host red cell. In addition, we are studying the impact of host iron supplementation on the growth and iron acquisition pathways of common pathogenic bacteria, including E. coli, Salmonella and S. aureus.
Our current work is conducted primarily in The Gambia in collaboration with the Medical Research Council Unit in Gambia (MRC-Gambia) and the MRC-International Nutrition Group. Please see this link for more information about this project: Safer Supplements
Trauma: We focus on the discovery of therapeutic molecules that down regulate the host response to infection and injury. EPO was first described as a renal hormone that stimulates erythropoiesis. We have shown that EPO has neuroprotective, anti-inflammatory, synaptogenic, and immunomodulatory activities and promotes the recruitment of stem cells after injury. We are currently investigating the use of EPO derivatives as neuroprotective agents for possible clinical use in traumatic brain injury and other types of neurological injury.
Clark M.A., Kasthuri R., Fulford A., Taylor S.M., Prentice A., Goheen M.M., Fisher N., Cerami C. Host iron status and iron supplementation conspire to mediate host susceptibility to erythrocytic stage of Plasmodium falciparum. Nature Communications. 2014 Jul 25;5:4446 PMID:25059846
Clark M.A., Goheen M.M., Spidale, N., Kasthuri R., Fulford A., Cerami C. RBC barcoding allows for the study of erythrocyte population dynamics and P. falciparum merozoite invasion. PLoS One. 2014 Jul 1;9(7):e101041. PMID:24984000
Clark M.A., Fisher N., Kasthuri R., Cerami, C. Erythrocyte stage P. falciparum bioavailable iron content changes with parasite maturation and responds to host serum iron. British Journal of Haematology 2013 Apr;161(2):262-9. PMID:23398516
Taylor S.M., Cerami C, Fairhurst R.M. Hemoglobinopathies: Slicing the Gordian Knot of Plasmodium falciparum Malaria Pathogenesis. PLoS Pathogens. 2013 May;9(5):e1003327. PMID: 23696730
Cerami C., Brines M. Tissue-protection by erythropoietin: Is a safe translation into the clinic possible? Journal of Investigative Medicine. Jul 30 2010 PMID: 20683348
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