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May Ho, MSc, MD, FRCPC

Professor, Department of Microbiology, Immunology & Infectious Diseases and Medicine

Microbiology, Immunology & Infectious Diseases (MIID)May Ho
Alberta Heritage Foundation for Medical Research Senior Medical Scholar
Immunology Research Group
Address: Health Research Innovation Centre
Phone: (403) 220-8516
Fax: (403) 210-8862

Curriculum Vitae:

  • BSc, McMasters University, 1967
  • MD, University of Toronto, 1971
  • MSc, University of London, United Kingdom, 1977


The research in my laboratory focuses on cytoadherence, the process by which Plasmodium falciparum -infected erythrocytes (IRBC) adhere to vascular endothelium, with resultant mirocirculatory obstruction, metabolic abnormalities and organ dysfunction. We use both a parallel plate flow chamber in vitro and the human/SCID mouse model in vivo to investigate the molecular basis of cytoadherence, and to assess potential anti-adhesive therapies. Studies are also under way to investigate the intracellular signalling events that occur in microvascular endothelial cells as a result of the adhesion of IRBCs to the host receptor CD36. Our data to date have shown that IRBCs roll and adhere on human microvessels in vivo. Adhesion is mediated by CD36, while interaction with ICAM-1 appears to stabilize the IRBC-CD36 interaction without increasing the number of IRBCs recruited to the endothelium. In contrast, induction of P-selectin expression increases the number of rolling IRBCs that subsequently adhere to CD36. These findings strongly support the paradigm we propose that cytoadherence is a multi-step process involving several adhesion molecules under physiological shear stress. We further demonstrated that a recombinant peptide (PpMC-179), from the parasite cytoadherent ligand PfEMP1, that corresponds to the minimal binding domain to CD36 can inhibit and even reverse the adhesion of IRBCs from diverse clinical isolates in vivo. The anti-adhesive effect of PpMC-179 is rapid and sustained in vivo for at least 30 minutes, suggesting that targeting cytoadhesion in vivo is feasible and may offer a rapid antimalarial therapy. The anti-adhesive effect of nitric oxide has also been studied. Inhibition of endogenous NO production enhances cytoadherence through the induction of P-selectin expression, while NO donors inhibit cytoadherence through the downregulatory effect of NO on ICAM-1 and VCAM-1 expression. Experiments are under way to investigate the role of NO in vivo in the human/SCID mouse model. Finally, our results on the induction of intracellular signaling in host endothelial cells by the PfEMP1-CD36 interaction suggest a novel mechanism for the modulation of cytoadherence under flow conditions through a signaling pathway involving CD36, Src-family kinases and an ecto-alkaline phosphatase. Targeting endothelial ecto-alkaline phosphatases and/or signaling molecules may constitute a novel therapeutic strategy against severe falciparum malaria.


Graduate Student
Shaun Davis
Mark Gillrie
Roxna Kapadia

Research Technician
Kristine Lee

Administrative Assistant
Florence Yang