Vascular Inflammation in Malaria Pathogenesis

The pathogenesis of malaria is characterized by vascular inflammation exacerbated by immune cells that travel to areas where red blood cells infected with parasites stick to the endothelium lining the blood vessels. The Lamb lab has made significant discoveries demonstrating a key role for receptor tyrosine kinase family Eph receptors in malaria pathogenesis. Continue reading → Vascular Inflammation in Malaria Pathogenesis

Research Statement

We work on malaria, a disease caused by infection Plasmodium parasites that invade the body’s red blood cells and can cause a harmful systemic infection.

We are particularly interested in factors affecting the generation of a robust immune response to kill and remove the infection. We also work on determining the molecular mechanisms mediating vascular activation during malaria. Vascular activation is a key event in organ-specific pathologies associated with Plasmodium-infected red blood cells sequestering on the endothelial cells lining the vasculature of the body.

By understanding the molecules that are required to kill and clear the numbers of Plasmodium infected red blood cells we will be able to design new therapies to enhance these mechanisms of parasite control. By understanding how the vasculature becomes inflamed and disrupted during malaria we will be able to design therapies that block these mechanisms of vascular leakage preventing some of the most severe symptoms of malarial disease.

We work on human malaria in collaboration with Dr Lawrence Ayong and Dr Carole Eboumbou of the Centre Pasteur Cameroon.

We also use a rodent models of malaria to dissect the mechanisms human malarial disease.

Lamb Lab