Maria Bernabeu

Thank you very much for highlighting our work. This is one of our first big stories coming from out the lab, so we are very excited!

📣Announcing the 4th edition of the EMBL‑IBEC Conference on “Engineering Multicellular Systems”, taking place 11–13 March 2026 in Barcelona. Exploring organoids, mechanobiology, embryo models, organ-on-chip systems, multiomics and more. Abstracts open now!
events.ibecbarcelona.eu/embl-ibec-co...

Huge thanks to @mariabernabeu.bsky.social and to everyone else who contributed and made this project possible 🎉

Thanks again @alinabatzi.bsky.social for a titanic work, and all the lab. @jamesasharpe.bsky.social lab and Lars Steinmetz lab for computational help. Miguel and Mireia at UPF for insights in immune-endothelial responses, and my ❤️ friend @moncunill.bsky.social, for getting us into deep immuno!

Our study shows the power of using bioengineered models in combination with deep single cell profiling to study complex immune responses.

For the first time, we can introduce different infection relevant drivers into human models to identify their individual role in tissue damage.

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

Innate immune responses to Plasmodium falciparum disrupt the blood-brain barrier Plasmodium falciparum accumulation at the blood-brain barrier (BBB) is a hallmark of cerebral malaria, a life-threatening complication. Conversely, the contribution of the immune response to vascular ...

Pre-print alert 🚨
We answer a longstanding question in the field. Do immune cells cause cerebral malaria?

The answer is YES!!!! And independently of P. falciparum accumulation in the brain.

www.biorxiv.org/cgi/content/...

Just hot out of the press! Rory developed a 3D microvessel model that recapitulates physiological pericyte coverage. We found that Plasmodium falciparum egress products disrupt the barrier and halt ang-1 secretion. The activator AKB-9778 could rescue barrier disruption! Congratulations, Rory!

I think I didn't 🙈 but @rorykmlong.bsky.social left everything ready, so there was a very minimum chance for me to screw up! ☺️

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.

Back from #ParaFrap! What a fantastic meeting. I feel very privileged to be part of this community! Specially in my heart the new generation of kickass PIs/GL ❤️ (mostly women dominated💪🏻)

This article highlights the importance of agressive antypiretic treatment in malaria infections and has potential consequences for other infections and brain injuries!!!!

We could reverse this highly negative effect by protecting the endothelial glycocalyx with Batimastat, an MMP1 inhibitor.

This effect was conserved in lung 3D microvessels, as well as an increase in neutrophil binding.

Just a short 30 min exposure to 40C, common in malaria patients, significantly increased parasite binding to 3D microvessels at multiple flow conditions. We found this occurred in several parasite lines with tropism in the brain, without apparent changes in their endothelial receptors EPCR and ICAM

Febrile temperature enhances Plasmodium falciparum cytoadhesion by disrupting the endothelial glycocalyx Fever, a universal host defense in infection and inflammation, paradoxically contributes to neurological complications in malaria. While febrile temperatures enhance the expression of parasite virulen...

Have you ever wondered what happens with your microvessels after exposure to high temperature in fever? In this preprint former postdoc (ans soon to be PI) Viola Introini found that high temperatures cleaves glycocalyx , having severe consequences in malaria www.biorxiv.org/cgi/content/...

We are searching for an enthusiastic scientist to join our team and establish annual killifish as a model system for early developmental biology and biophysics! @embl.org @embldbunit.bsky.social

Apply here:
embl.wd103.myworkdayjobs.com/EMBL/job/Hei...

Please re-post 🙏

It has been amazing that you were my (co-)first PhD student. Amazing journey. You should be proud of everything you achieved

A big thanks to everyone, who contributed to the project.To the full Bernabeu group, as this was a team project! As well as our @embl.org collaborators @jamesasharpe.bsky.social group, @yschwab.bsky.social's team and Lars Steinmetz group!

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 egress disrupts endothelial junctions and activates JAK-STAT signaling in a microvascular 3D blood-brain barrier model Nature Communications - Here the authors show that Plasmodium falciparum egress products disrupt endothelial barrier and activate JAK-STAT and interferon type response in a 3D blood-brain barrier...

We are happy to show one ourt first exciting papers. We have developed a blood-brain barrier model to study the disruptive effects caused by the malaria parasite, Plasmodium falciparum.

First, congratulations to the fearless @liviapiatti.bsky.social and @alinabatzi.bsky.social

rdcu.be/ezBl7

Congratulations! Great work!

The essential host genome for Cryptosporidium survival exposes metabolic dependencies that can be leveraged for treatment An arrayed microscopy-based CRISPR screen revealed host genes affecting multiple infection phenotypes of the intracellular parasite Cryptosporidium. Hits in the host cholesterol biosynthesis pathway a...

Our paper has finally graduated from pre-print to peer-reviewed, pretty much unscathed, and is out now! www.cell.com/cell/fulltex...

Finally, an unexpected but valuable contribution from ppolinski.bsky.social‬ and @viktri08.bsky.social ‬ showing remarkable alterations on endothelial splicing caused by the malaria products.