Alina finally integrated the scRNAseq immune dataset with our recently published dataset of the 3D-BBB model being exposed to P. falciparum. We identified shared and dominant disrupted pathways (JAK-STAT!) in all cells. As well as parasite/immune-specific disruptive pathways on endothelial cells.

Barrier disruption was mostly mediated by locally acting granzyme B and IFNy secreted by gd T cells and NK cells. We could prevent barrier disruption by preventing immune cell binding with anti-ICAM-1 antibodies.

More important, P. falciparum-stimulated immune cells cause BBB disruption, making the barrier leakier through decrease junctional VE-cadherin, increase contractility and apoptosis

Monocytes, gd T cells and NK cells cells secrete TNFa and IFNg, causing a strong inflammation and activation of all BBB cells, accounting for 20% of changes in the transcriptome.

In a project spearheaded by the relentless @alinabatzi.bsky.social, we used an immunocompetent 3D-Blood brain barrier (BBB) model and found that Plasmodium falciparum stimulated immune cells accumulate much more to the BBB (mostly T-cells), driven by changes on LFA high-affinity conformation

Then and now... 2022. Helping @rorykmlong.bsky.social and François on midnight experiments. 2025 Helping Rory to finish experiments for François' paper revision. Bonus points: The surprise of new lab members when they found me in the TC room after being > 1 year at my desk.

More important, we could reverse the increase in vascular barrier permeability induced by malaria products with Ruxolitinib, a JAK-STAT inhibitor! This is super exciting with the drug now being tested in CHMI studies. www.medrxiv.org/content/10.1...

We also found that falciparum egress products activate interferon and antigen presenting pathways in all the cells that compose the BBB, endothelial, astrocytes and pericytes. Including JAK-STAT as one of the key signaling inflammatory hubs

The release of malaria products during egress leads to BBB disruption, including downregulation of tight and adherens junctional proteins as well as key vascular development pathways. This effect is localized at sites where parasites egress.

Plasmodium falciparum shows increased binding to ETS-endothelial cells. Exposure to parasite products caused a disruption on the endothelial barrier and we reveal a sustained and global downregulation of junctional, cytoskeletal and focal adhesion genes

Pre-print alert 🚨: We have developed 2D and 3D stable iPSC endothelial-differentiation models through dox inducible ETS expression. We demonstrate endothelial identity and used these models for studying malaria pathogenesis research. www.biorxiv.org/content/10.1...

Because not all is work...Yesterday we took the opportunity that almost all lab members were around and had a super fun fanta blind testing activity courtesy of Viola Introini!

Congratulations to Dr. Rory Long, who successfully defended his thesis yesterday! Rory pulled out his project independently, and found that malaria products decrease secretion of Ang-1 in brain pericytes in complex 3Dmodels, and tested therapies that restore ang-Tie2 axis. Cannot be more proud!!!

The @mimsumea.bsky.social , @scilifelab.se and @embl.org workshop "infection across scales" was a success. Special thanks to @mimsumea.bsky.social Oliver and Nora for being fantastic hosts and organizing once in a lifetime networking activities.

We are very excited to announce a new @events.embl.org conference with a general focus on all infections with the goal to foster discussions across researchers working on multiple pathogens. We couldn't find a conference as such in Europe, so we decided to organize it 😊

www.embl.org/about/info/c...

Congratulations @liviapiatti.bsky.social on a fantastic thesis and great defense. Super proud of you!