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Dr Teresa Tiffert

My research is concerned with the mechanisms that mediate and control ion traffic across biological membranes in health and disease. We investigate the physiological and pathophysiological changes in ion transport and in the homeostatic condition of human red blood cells during circulatory aging, and in diseases such as sickle cell anaemia and malaria.
Dr Teresa Tiffert

University Senior Lecturer

Office Phone: +44 (0) 1223 333747

Research Interests

My current research interests are focused on the blood stages of falciparum malaria. Our discovery that the invasion efficiency of falciparum parasites was markedly reduced by red cell dehydration (Blood,105:4853-4860, 2005) proved relevant to the understanding of the mechanisms by which inherited haemolytic anaemias with gene pools sustained in malaria-endemic regions, protect individuals against severe malaria.  In many of these anaemias, the presence of dehydrated, dense subpopulations of red cells in the circulation prevents the development of high parasitaemias, a pre-condition for disease severity. Our search for possible mechanisms of density-protection focused attention on an elusive pre-invasion stage of parasite-red cell interaction, during which falciparum merozoites align apically, ready to penetrate and infect red cells (Trends Parasitol. 23:481-48, 2007). This is the least understood stage of the invasion process. Elucidation of its mechanism may pave the way to novel malaria therapies. Investigation of the pre-invasion stage poses formidable technical challenges which we are currently trying to overcome in a multidisciplinary collaboration with colleagues from the Department of Physiology, Development and Neuroscience, the Cavendish Laboratory and the Wellcome Trust Sanger Institute (Biophys. J. 107:846-853, 2014).


Dr Virgilio Lew, Department of Physiology, Development and Neuroscience, University of Cambridge

Dr Pietro Cicuta, Cavendish Laboratory, University of Cambridge

Dr Julian Rayner, Wellcome Trust Sanger Institute, Hinxton, Cambridge


Course organiser: IA MVST Histology

Key Publications

Lew VL, Tiffert T, (2015), Volume control in Plasmodium falciparum-infected red blood cells, Encyclopedia of Malaria, Springer, DOI 10, 1007/978-1-4614-8757-9_27-1

Crick AJ, Theron M, Tiffert T, Lew VL, Cicuta P, Rayner JC, (2014), Quantitation of malaria parasite-erythrocyte cell-cell interactions using optical tweezers, Biophys. J, 107:846-853

Tiffert T, Lew VL, (2014), Dynamic morphology and cytoskeletal protein changes during spontaneous inside-out vesiculation of red blood cell membranes, Pflugers Arch - Eur J Physiol, DOI 10.1007/s00424-014-1483-5

Crick AJ, Tiffert T, Shah SM, Kotar J, Lew VL, Cicuta P, (2013), An automated live imaging platform for studying merozoite egress-invasion in malaria cultures, Biophys. J, 104:997-1005

Tiffert T, Lew VL, (2011), Elevated intracellular Ca2+ reveals a functional membrane nucleotide pool in intact human red blood cells, J. Gen. Physiol, 138(4): 381-391

Mauritz JMA, Seear R, Esposito A, Kaminski CF, Skepper JN, Warley A, Lew VL, Tiffert T, (2011), X-ray microanalisis investigation of the changes in Na, K, and haemoglobin concentration in Plasmodium falciparum-infected red blood cells, Biophys. J, 100:1438-1445

Esposito A, ChoimetJ-B, Skepper JN, Mauritz JMA, Lew VL, Kaminski CF, Tiffert T, (2010), Quantitative imaging of human red blood cells infected with Plasmodium falciparum, Biophys. J, 99:1-8

Mauritz JMA, Esposito A, Ginsburg H, Kaminski CF, Tiffert T, Lew VL, (2009), The homeostasis of Plasmodium falciparum-infected red blood cells, PLoS Computational Biology, 5(4):e1000339

Esposito A, Tiffert T, Mauritz JMA, Schlachter S, Bannister LH, Kaminski CF, Lew VL, (2008), FRET imaging of hemoglobin concentration in Plasmodium falciparum-infected red cells, PLoS ONE, 3(11):e3780

Lew VL, Tiffert T, (2007), Is invasion efficiency in malaria controlled by pre-invasion events?, Trends Parasitol, 23:481-484

Tiffert T, Daw N, Etzion Z, Bookchin RM, Lew VL, (2007), Age-decline in the activity of the Ca2+-sensitive K+ channel of human red blood cells, J. Gen. Physiol, 129:429-436

Tiffert T, Lew VL, Ginsburg H, Krugliak M, Croisille L, Mohandas N, (2005), The hydration state of human red blood cells and their susceptibility to invasion by Plasmodium falciparum, Blood, 105:4853-4860

Lew VL, Tiffert T, Ginsburg H, (2003), Excess hemoglobin digestion and the osmotic stability of Plasmodium falciparum-infected red blood cells, Blood, 101:4189-4194

Above: Electron-probe x-ray microanalysis maps of the elemental distributions of Na, K, and Fe in uninfected red blood cells and in red blood cells infected with P. falciparum malaria parasites at the mature trophozoite stage. The figure illustrates the dramatic changes in the ion composition of red blood cells, induced by P. falciparum infection. There is dissipation of the normal Na/K gradients across the red cell membrane, whereas the parasite cytoplasm retains a typical high-K, low-Na intracellular environment. The electron microscopic images (top row) are shown vertically aligned with the corresponding X-ray images (bottom row). The X-ray maps are assembled as a red-green-blue overlay of the Na (green), K (red), and Fe (blue) X-ray raw peak count for each spot. Mixtures of these colors can result, e.g., in yellow (both high K and Na), or violet (both high Fe and K). (A and B) Uninfected red blood cell surrounded by salt crust from the dried extracellular medium. (C and D) Infected red blood cell with a mature trophozoite and food vacuole. The black spots are hemozoin crystals responsible for the high Fe signal. (E and F) Infected red blood cell with a mature trophozoite, next to two uninfected red blood cells (white starred). (Biophysical Journal 100(6): 1438–1445, 2011).