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

(7/7)

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)

all the other co-authors, students and colleagues, who made this possible: @mariazalmeida.bsky.social , Teresa Porqueddu, Viola Introini, @silviasanzsender.bsky.social, and Diana Carrasqueira (5/5)

- @marianadeniz.bsky.social, our long-term collaborator who never drops the ball and is always ready for new scientific adventures
- @aitorcasass.bsky.social, who accepted my crazy, time-constrained request of playing with tsetse flies, in a déjà-vu from our joint PhD time (4/5)

- the utterly supportive @luisamfigueiredo.bsky.social , who has encouraged me during my postdoc in her lab to push boundaries and not give up, and has allowed me to take this project forward to my lab (3/5)

Thanks to:
- @mariabernabeu.bsky.social , who spearheaded the microvessel technology in malaria, fully embraced my desire to adapt it to trypanosomiasis, and adopted me in her lab for a few amazing months (2/5)

Congratulations!!