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Pedro Escoll

@pescoll.bsky.social

How the metabolic crosstalk between pathogenic bacteria and host cells impacts infection? @pasteur.fr

22 Posts88 Follower111 Folgt
Jean-Yves Tinevez@jytinevez.bsky.social · 10mo ago

Job alert! We are looking for a bioimage analysis to work in an image analysis core facility in beautiful Paris. Can I ask you to share this opportunity with your networks? See also on the forum: forum.image.sc/t/research-e...

Research engineer in Bioimage Analysis for the researchers of the inIdEx FORMULA

Hi all We are looking for a bioimage analysis to work in an image analysis core facility in beautiful Paris. Can I ask you to share this opportunity with your networks? The position is in the Instit...

forum.image.sc

Pedro Escoll@pescoll.bsky.social · 11mo ago

New preprint in the lab! How the mitochondrial ETC works during infection of human macrophages with #Legionella or #Salmonella? Spoiler: there are some similarities and also pathogen-specific differences. Work led by Francisco Garcia and Paula Martínez, with @cbuch.bsky.social at @pasteur.fr

Figure 5. Working model for pathogen-specific ETC modulations that preserve the ∆ψm in hMDMs. (A) L. pneumophila: T4SS effectors dampen OxPhos early during infection and preserve the ∆ψm by engaging the reverse mode of the FOF1 -ATPase. The ∆ψm remains high enough that ANT stays in forward mode, limiting cytosolic ATP drain. All ETC complexes (I-IV) contribute to maintaining the ∆ψm. Complex I is uniquely essential during WT infection. (B) S. Typhimurium: T3SS SPI-1/2 effectors reduce respiration and preserve the ∆ψm without inducing the reverse mode of the FO F1 -ATPase. Virulent bacteria rely on Complex I-driven electron entry with obligatory Complex III/IV proton pumping, while Complex II contributes in all infection conditions. Secretion-defective mutants fail to establish the Complex I-dependent configuration.
bioRxiv Microbiology@biorxiv-microbiol.bsky.social · 11mo ago

Complex-I Preserves Mitochondrial Polarization during Infection of Human Macrophages by Secretion-competent Bacteria https://www.biorxiv.org/content/10.1101/2025.09.04.674018v1

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

Zeynep Baharoglu@zeynepbaharoglu.bsky.social · 11mo ago

So excited our antibiotic potentiation story is out 🤩 Led by the extraordinary @manonlang.bsky.social with @fox-science.bsky.social & @amazeld.bsky.social +amazing collaborators @immunobladder.bsky.social @imaneelmeouche.bsky.social 🦠 We believe it can make a difference in #AMR infections!

Uridine as a potentiator of aminoglycosides through activation of carbohydrate transporters

Uridine boosts aminoglycoside treatment efficiency against antibiotic-susceptible as well as antibiotic-resistant E. coli strains.

science.org

Pedro Escoll@pescoll.bsky.social · 11mo ago

New preprint in the lab! How the mitochondrial ETC works during infection of human macrophages with #Legionella or #Salmonella? Spoiler: there are some similarities and also pathogen-specific differences. Work led by Francisco Garcia and Paula Martínez, with @cbuch.bsky.social at @pasteur.fr

Figure 5. Working model for pathogen-specific ETC modulations that preserve the ∆ψm in hMDMs. (A) L. pneumophila: T4SS effectors dampen OxPhos early during infection and preserve the ∆ψm by engaging the reverse mode of the FOF1 -ATPase. The ∆ψm remains high enough that ANT stays in forward mode, limiting cytosolic ATP drain. All ETC complexes (I-IV) contribute to maintaining the ∆ψm. Complex I is uniquely essential during WT infection. (B) S. Typhimurium: T3SS SPI-1/2 effectors reduce respiration and preserve the ∆ψm without inducing the reverse mode of the FO F1 -ATPase. Virulent bacteria rely on Complex I-driven electron entry with obligatory Complex III/IV proton pumping, while Complex II contributes in all infection conditions. Secretion-defective mutants fail to establish the Complex I-dependent configuration.
bioRxiv Microbiology@biorxiv-microbiol.bsky.social · 11mo ago

Complex-I Preserves Mitochondrial Polarization during Infection of Human Macrophages by Secretion-competent Bacteria https://www.biorxiv.org/content/10.1101/2025.09.04.674018v1

Andreas Bäumler@abaumler.bsky.social · 12mo ago

A Salmonella T3SS-2 mutant grows fine in spleen macrophages, contradicting tissue culture dogma (PMID: 23236281). This observation was largely ignored, but adding certain carbon sources rescues growth in cultured macrophages, hinting that T3SS-2 may be doing something entirely different in vivo.

Pedro Escoll@pescoll.bsky.social · last yr.

New pre-print in the lab! Beautiful work by Francisco Garcia-Rodriguez in collab with @kamovalenz.bsky.social and @joaquinbernal.bsky.social : when macrophages are provided with specific nutrients, Salmonella can bypass its requirement of the T3SS to replicate, a process that occurs within the SCV

Pedro Escoll@pescoll.bsky.social · last yr.

New pre-print in the lab! Beautiful work by Francisco Garcia-Rodriguez in collab with @kamovalenz.bsky.social and @joaquinbernal.bsky.social : when macrophages are provided with specific nutrients, Salmonella can bypass its requirement of the T3SS to replicate, a process that occurs within the SCV

bioRxiv Microbiology@biorxiv-microbiol.bsky.social · last yr.

Provision of Preferred Nutrients to Macrophages Enables Salmonella to Replicate Intracellularly Without Relying on Type III Secretion Systems https://www.biorxiv.org/content/10.1101/2025.05.15.653970v1

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.
Pedro Escoll@pescoll.bsky.social · last yr.

New pre-print in the lab! Beautiful work by Francisco Garcia-Rodriguez in collab with @kamovalenz.bsky.social and @joaquinbernal.bsky.social : when macrophages are provided with specific nutrients, Salmonella can bypass its requirement of the T3SS to replicate, a process that occurs within the SCV

bioRxiv Microbiology@biorxiv-microbiol.bsky.social · last yr.

Provision of Preferred Nutrients to Macrophages Enables Salmonella to Replicate Intracellularly Without Relying on Type III Secretion Systems https://www.biorxiv.org/content/10.1101/2025.05.15.653970v1