Decoding Blood Brain Barrier Endothelial Responses to parasitic infection: Omics Driven Mapping of Receptor and Transporter Dynamics

About the Project

The blood–brain barrier (BBB) has been described as the final and last frontier for medicine. Delivering drugs to the brain is a major challenge, particularly for large molecules and biologics. The restrictive BBB prevents all but small (<450 Da) or lipid‑soluble drugs from entering the brain, due to a combination of robust tight junctions between capillary endothelia, active multi‑drug efflux transport and drug‑metabolising enzymes.

Building on our established BBB platforms, this PhD project will focus on parasitic pathogens of neurological relevance, specifically Toxoplasma gondii and Acanthamoeba, to interrogate how infection perturbs endothelial receptor and transporter expression that governs barrier selectivity.

The central objective is to establish parasite infection‑based in vitro BBB models and define infection‑driven changes in key influx, efflux and adhesion machinery (e.g., GLUT1, LAT1, transferrin receptor, claudins and occludin). Quantitative ‘omics’ readouts, label‑free LC‑MS/MS proteomics and bulk RNA‑seq transcriptomics, will be integrated with functional metrics including TEER, paracellular permeability and targeted transport assays.

Knowledge exchange, training and method transfer will be delivered through collaboration with Kings College London (KCL), ensuring robust model development, high‑quality analytical workflows and translational relevance.

Project Aims:

1. Technology-transfer robust BBB transwell and co-culture model systems into Strathclyde through collaboration with KCL achieving high TEER and low paracellular permeability using porcine and, where appropriate, other tissues.
2. Establish controlled infection of BBB endothelial–glial models with T. gondii and Acanthamoeba; quantify parasite burden and localisation within endothelial and glial compartments.
3. Profile infection-driven modulation of endothelial receptor and transporter expression using transcriptomics (RNA-seq) and quantitative proteomics.
4. Validate functional consequences of omics-identified shifts through permeability assays (e.g., fluorescent dextrans), TEER monitoring, and targeted transport assays

To apply please send a CV and cover letter, detailing your motivation to pursue this project to c.w.roberts@strath.ac.uk