Abstract
Neural Trypanosomiasis is fatal disease caused by Trypanosoma brucei. T. brucei complex consists of three major subspecies namely T. brucei brucei, T. brucei gambiense, T. brucei rhodesiense. They are transmitted by the saliva of the infected tsetse flies of genus Glossina during blood meal. Trypanosomas are extracellular, spread through the blood stream to various niches, and consequently invade the central nervous system (Masocha et al., 2007). It is necessary to know how T. brucei interacts with brain microvascular endothelial cells (BMECs) to cross the blood brain barrier. Previous studies have shown that majority of extracellular pathogens have to adhere to BMEC first (transient adhesion), which then induces series of cell events causing more firm adhesion of pathogen to BMECs (stationary adhesion), followed by alteration in the extracellular matrix near tight junctions allowing more space for pathogen to cross BBB (reviewed in Bencurova et al. 2011). To this background, the study was aimed to identify putative surface adhesion receptors on BMECs that may take part in the Trypanosoma:BMEC interface during transient adhesion. Unfolding the underlying principles of ligand:receptor interactions, which take place during passage of Trypanosoma through BBB is important to understand its neuroinvasive mechanisms.
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