RT

Kimberly Kline 🏔@kimingeneva.bsky.social · 5mo ago

What if quorum sensing doesn’t promote biofilms - but restrains it? 🤔 New work from @harisantypas.bsky.social shows that the Fsr QS system in Enterococcus faecalis acts as a brake on biofilm formation and pathogenesis during infective endocarditis (IE). www.nature.com/articles/s41...

What if quorum sensing doesn’t promote biofilms - but restrains it? 🤔 New work from @harisantypas.bsky.social shows that the Fsr QS system in Enterococcus faecalis acts as a brake on biofilm formation and pathogenesis during infective endocarditis (IE). www.nature.com/articles/s41...

Loss of Fsr quorum sensing promotes biofilm formation and worsens outcomes in enterococcal infective endocarditis - Nature Communications

Infective endocarditis (IE) is an understudied biofilm-associated infection. Here, analyses of preclinical and clinical data reveal that the Fsr quorum sensing (QS) system of Enterococcus faecalis is ...

nature.com

Enterococcus fans: Check out our latest on E. faecalis EET, advancing our understanding of both the fundamental physiology of this bug and new mechanisms of its virulence. This is the product of a thrilling collaboration with friends in Singapore @gthibault.bsky.social led by @aarontan.bsky.social.

Guillaume Thibault@gthibault.bsky.social · 7mo ago

We’ve discovered how the superbug E. faecalis prevents chronic wounds from healing. It’s not a toxin. It’s metabolism. The bacteria use extracellular electron transport (EET) to electrochemically generate ROS, effectively "freezing" skin cells in place. doi.org/10.1126/sciadv.aeb5297

Strep/Enterococcal colleagues! Streptococcal Biology GRC/GRS are open for applications. Acceptances are underway and the meeting is on track to fill up. If you’re aiming for a short talk (lots of slots), registering early matters for full consideration. Share widely! www.grc.org/streptococca...

Our latest efforts to understand Enterococcal wound infection. In long-term collaboration with @gthibault.bsky.social, we discovered how E. faecalis makes extracellular ROS - via EET!⚡️Which in turn dysregulates host UPR to delay wound healing. Led by @aarontan.bsky.social - his videos below are 🤩!

Guillaume Thibault@gthibault.bsky.social · 12mo ago

📢 Our new preprint is out! We show how the common gut bacterium 𝘌. 𝘧𝘢𝘦𝘤𝘢𝘭𝘪𝘴 stops wound healing. It uses a metabolic pathway, extracellular electron transport (EET), to stress host cells, halting their migration. Watch WT bacteria (orange) stop the cells while the mutant (blue) doesn't!