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Enninga Lab

@enningalab.bsky.social

Dynamics of Host-Pathogen Interactions Unit at @pasteur.fr https://research.pasteur.fr/en/team/dynamics-of-host-pathogen-interactions/

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Enninga Lab@enningalab.bsky.social · 11mo ago

Time for some insights into our latest #preprint Using cryo–electron tomography, we peeked inside different #Mtuberculosis strains, and a couple of other mycobacteria.🧐 Surprise: some species, especially the host-adapted ones, build intracytoplasmic membranes (we call them MIMs)! 🦠

Enninga Lab@enningalab.bsky.social · 11mo ago

🦠 Mycobacteria aren't just tough, they're interior designers! 🦠 Check out our latest #preprint 🚨, led by our PhD student @camimille.bsky.social , where we show that #Mycobacterium tuberculosis builds secret cytoplasmic membranes to adapt its metabolism and sneak past immunity 🤫 Thread coming soon!

Enninga Lab@enningalab.bsky.social · 11mo ago

🦠 Mycobacteria aren't just tough, they're interior designers! 🦠 Check out our latest #preprint 🚨, led by our PhD student @camimille.bsky.social , where we show that #Mycobacterium tuberculosis builds secret cytoplasmic membranes to adapt its metabolism and sneak past immunity 🤫 Thread coming soon!

bioRxiv Microbiology@biorxiv-microbiol.bsky.social · 11mo ago

Nitrate-responsive Mycobacterial Intracytoplasmic Membranes dampen Inflammation during Mycobacterium tuberculosis Infection https://www.biorxiv.org/content/10.1101/2025.09.17.676823v1

Enninga Lab@enningalab.bsky.social · last yr.

So cool to see our recent @plosbiology.org paper from Léa explained in French 🇫🇷🥖 cryo CLEM is more fun than google earth!

Institut Pasteur | 130 years of biomedical research@pasteur.fr · last yr.

Zoom into a human cell infected by Shigella, the bacteria behind dysentery. Using cryo-EM, @leaswistak.bsky.social and team revealed how it pierces cells with molecular syringes. Stunning science at the nanoscale. @enningalab.bsky.social @jytinevez.bsky.social @nanoimaging.bsky.social #CryoEM

Enninga Lab@enningalab.bsky.social · last yr.

Our latest paper is out! Congratulations to @leaswistak.bsky.social et al for this amazing #cryoET work that elucidates the initial stages of #T3SS dependent vacuolar damage during #Shigella infection. We will do a deep-dive later! journals.plos.org/plosbiology/...

The bacterial type three secretion system induces mechanoporation of vacuolar membranes

Many intracellular bacteria breach vacuolar membranes to replicate in the host cytosol, but the precise mechanisms remain unclear. This study shows that the human pathogen Shigella flexneri uses its t...

journals.plos.org

PLOS Biology@plosbiology.org · last yr.

How do intracellular #bacteria breach vacuoles to enter the host cytosol? @leaswistak.bsky.social @matthijnvos.bsky.social @enningalab.bsky.social &co show that #Shigella uses its T3SS system to damage endomembranes via mechanoporation to initiate cytosolic access @plosbiology.org 🧪 plos.io/4jXrr9Z

Left: Group of three T3SS localizing in the same zone of the bacteria surface. T3SS n°1 and 2 contact, deform, and perforate the vacuole membrane at the same spot. T3SS n°1 needle (83 nm) is long and seems to deviate from basal body axis showing that strong constraints between T3SS and the vacuole at are play. The locally relaxed vacuole to bacteria space (~50–55 nm) potentially limits additional damage by the T3SS n°3 needle (56 nm) that only slightly deforms the membrane. Right: Model of initial vacuolar membrane breaching by T3SS-induced mechanoporation. Shigella actively enters host cells in a specialized endomembrane compartment, the vacuole, that is rapidly injured and ruptured for cytosolic access. After host cell entry, the vacuole membrane is intact and tightly juxtaposed to the surface of Shigella, permitting contact between T3SSs and the endomembrane. In the authors’ proposed model, vacuole membrane injury is supported both by the vacuole tightness and the length of individual T3SSs.