Free Republic
Browse · Search
General/Chat
Topics · Post Article

To: neverdem

Interesting. I wonder what the mechanism of action is.

The penicillins work by inhibiting bacterial cell wall polymerization. Bacteria counter this with the beta-lactamase enzyme, which cuts open a ring structure in the penecillins, making them ineffective.

Erythromycin has a completely different mode of action. It stops protein synthesis by interacting with the ribosome. Bacteria have different ways of countering this.

I find the idea of a protein-lipid complex that restores antibiotic sensitivity to such widely different antibiotics in bacteria having such different mechanisms of resistance rather amazing. Too amazing, in fact. I’d really like to see more studies and find out what is really going on here. It’s possible that all of the antibacterial activity is due to the protein complex and none of the antibiotics are necessary at all. But since bacteria will still grow in breast milk, this protein complex must be at very low concentration in milk.

Never mind me here. I’m just thinking out loud, trying to figure this out. Maybe I should just read the paper...


7 posted on 05/30/2013 5:25:58 PM PDT by exDemMom (Now that I've finally accepted that I'm living a bad hair life, I'm more at peace with the world.)
[ Post Reply | Private Reply | To 1 | View Replies ]


To: exDemMom; Mother Abigail; vetvetdoug; Smokin' Joe; Global2010; Battle Axe; null and void; ...
Receptor Proteins Hold Clues to Antibiotic Resistance in MRSA, Scientists Say FReebie

Immune Protein Could Stop (Type 1) Diabetes in Its Tracks, Discovery Suggests

FReepmail me if you want on or off my combined microbiology/immunology ping list.

9 posted on 05/30/2013 6:23:08 PM PDT by neverdem (Register pressure cookers! /s)
[ Post Reply | Private Reply | To 7 | View Replies ]

Free Republic
Browse · Search
General/Chat
Topics · Post Article


FreeRepublic, LLC, PO BOX 9771, FRESNO, CA 93794
FreeRepublic.com is powered by software copyright 2000-2008 John Robinson