I’ve written often (here and here, just for starters) how we have not developed new methods to eradicate infections from our bodies.  We use microbes to fatten our animals- cattle, chicken, etc.- because we’ve learned that putting antibiotics in animal feed not only keeps many infections at bay- even if they are not ready to invade the livestock- but feeding the antibiotics makes the animals gain weight- fast.  Which cuts the amount of time farmers and ranchers need to maintain the animals before they are slaughtered for our food.

Which also means that microbes are always seeing these antibiotics.  The therapies we need when these microbes invade humans and make us sick.  But, since the microbes have the opportunity (since the antibiotics are fed to the animals) to adapt to those (now useless) tools, the antibiotics are not effective in humans.

And, we haven’t developed new antibiotics in a long time.  It’s not that we haven’t been trying (ok, maybe not hard enough), but because we haven’t found what avenues of approach will work.  Ones that will stop the invading microbes cold.   Until now.

First, a little science.  (Please don’t give up yet.  I’ll try to keep this pretty simple.)  There are two kinds of microbes.  (No, not really.  There are tons of different microbes.  But, one of the differentiations we use, one that has been around for a long time, is how microbes react to what we call a Gram Stain.  If a microbe has a thick cell wall (peptidoglycan), it will be stained purple by crystal violet.  Gram negative microbes have a much thinner peptidoglycan wall, so they don’t stain purple; they are counterstained pink by safranin.)

And, Gram negative microbes have an inner cell membrane (which keeps all the cellular materials inside the cell) and an outer membrane.  It’s this outer membrane that seems to provide resistance to our antibiotics.  (Yes, it does mean that Gram positive microbes don’t seem to be resistant to antibiotics.)

Moreover, it seems that microbes have the same outer membrane structure on their mitochondria (the cell’s powerhouse; cellular components are produced here).  And, they are also found on chloroplasts (structures that contain the chlorophyll in plant cells that afford the ability to effect photosynthesis- the use of light energy to to convert carbon dioxide in the atmosphere to sugars).

It turns out that the outer membrane has proteins that help various materials enter and exit the cells.   And, Drs. Y. Gu, H. Li, H. Dong, Y. Zeng, Z. Zhang, N.G. Patterson, P.J. Stansfield, Z. Wang, Y. Zhang, W. Wang, and Dr. C. Dong [senior author] of East Anglia (Norwich, UK)  have discerned how these outer membrane proteins (OMP) operate.  They reported their results in Nature.

Which means we now can study how to stop microbial cells from growing.  Which will render the microbes susceptible to drugs and killing.   (We might also be able to stop microbial mitochondria to cease functioning, also killing the cells.)

What is the mechanism?  The researchers discerned the action by studying Escherichia coli (E coli), a ubiquitous Gram negative microbe.  The OMP are assembled within the cell, from which they are transported to the inner membrane.  Now, BAM (beta-barrel assembly machinery) then insert these OMPs into the outer cell membrane. When these OMP form gates, the cells are safe from outside attack.

Now, all we have to do is find out how to stop the BAM (or at least the first six strands of the barrels) from making those gates.   This would cripple the cells and render them unable to attack humans.

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