Oh, no, Roy. Another article about antibiotic resistance?
Of course, because it’s darned important. We need viable antibiotics to ensure that our populations stay healthy. And, if we don’t solve this dilemna- or create a slew of new antibiotics- we are going to be in a world of hurt. Literally.
Which is why this new research from the international group led by Dr. CA Arias (Texas Health Science Center, Houston) with his fellow researchers A Khan [doctoral student], D Panesso, WR Miller, L Diaz MR Cruz, AH Nguyen, SD Siegel, KV Singh, DA Garsin, and TT Tran (also from U Texas); Drs. M Davlieva, O Pemberton, and Y Shamoo (Rice); Drs J Reyes, S Rincon, and R Rios, (University of El Bosque); Dr. PJ Planet, (U Penn); Dr. A Narachania, (American Museum of Natural History), Dr. M Latorre, (University of Chile), and Dr. H Ton-That, (UCLA) is so important. Their research results, Antimicrobial sensing coupled with cell membrane remodeling mediates antibiotic resistance and virulence in Enterococcus faecalis were presented in PNAS (Proceedings of the National Academy of Sciences).
E. faecalis is one of the resistant microbes (it’s often termed vancomycin-resistant enterococci, VRE) that we’ve had a hard time eradicating. (It’s killed about 5500 folks, and ‘visited” some 55K folks last year in the US alone.) And, this new research detailed how the microbe senses- and then evades- antibiotics and immune system responses. This is a critical juncture- it may mean we’ve found the “Achilles’ heel”, the weak link in the chain that will let us address these superbugs.
As I reported a few weeks ago, many of these superbugs have found ways to avert the interference our antibiotics provide to their cell walls and membranes. (Out of the Box, 3 December 2019.) In this case, the VRE produces a protein (LiaX) that notifies it when antibiotics are in the environment- and that triggers them to restructure their cell wall to make it impervious to the attack. (In this case, the antibiotic was daptomycin- which has been effective against VRE- which mode of attack seems to be the middle of the cell, where the microbe divides, and by attaching there the cell dies. The VRE use LiaX to subvert this death knell event.)
It turns out LiaX not only serves as the ‘canary in the coal mine’, letting the cell know when there are antibiotics present, but also when the (patient) body’s immune response produces anti-microbial peptides (AMP’s) that destroy the cell envelope. By sensing either of those actions, it sends the message to protect the VRE form the ‘invader’- the item that will kill the VRE.
This means developing a target that terminates the action or production of LiaX should remove the resistance the invader manifests.
Tomorrow, we’ll talk about why this may not happen. (That will be the last on this subject for a while.)
Are our bodies getting more resistant to antibiotics nor are the strains just getting harder to kill. LiaX, I like that name 🤗
It’s not ourselves- because, then, we’d not be getting sick. It’s the microbes that are learning to develop “bulletproof vests” to protect themselves, Martha!
OK, Roy… thanks for the bad news! LOL.
Is this preventable? What is ‘Science’ doing to stop this? Do I show up tomorrow to get my answers? Such a cliff-hanger!
Thanks.
Paul.
Paul Taubman recently posted..Self-Sabotaging Behaviors That Keep You From Earning What You’re Worth
Actually, if a microbe could do this to protect itself…. what can a human do?
Very interesting. This is the first time that I could actually picture a war going on inside our bodies and the enemy could counter-attack. It will be interesting to see how fast they can put this research into action and start tearing down the walls the enemy puts up.
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I’m with you- how fast can we translate this to practical advantage. We need to deal with these (increasing numbers) of antibiotic resistant pests!