Our amazing student @leonorloira.bsky.social presented some of the lab’s work today at the @parafrap.bsky.social #EMBOconference
We are very proud.

At the #Parafrap #EMBO Conference “Host–Parasite Relationship: from Mechanisms to Control Strategies” in Ile des Embiez — amazing science, great friends, and stunning views! 🧬🌊✨

5. The profile of VSG expression in mouse models is altered in sequestered parasites.

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4. Both sequestered and non-sequestered parasites are infective to tsetse flies, but sequestered parasites result in heavier fly midgut infections. Whether this is linked to increased transmission potential remains unclear.

(6/7)

3. Sequestered parasites divide more than non-sequestered parasites in vitro and in vivo, regardless of the parasite strain.

(5/7)

2. cAMP Phosphodiesterase inhibition prevents and reverts parasite attachment to endothelial cells, suggesting that cAMP homeostasis is essential for sequestration.
(4/7)

What did we find?
1. Sequestration depends on wall shear stress/flow velocity, parasite strain, and endothelial cell type.

(3/7)

What's the problem?
using animal models is hard to decouple sequestration-derived events from general host responses.

So, what did we do?
We engineered 3D bovine microvessel models that mimic the bovine brain microvasculature and the bovine aorta.

(2/7)

We developed two systems of artificial bovine vasculature and we used them to study how trypanosome parasites attach to blood vessels.