How Do the Microbiota Communicate with Their Host? Scientists Have Cracked the First Mechanism!

I don’t know if you remember but back in  December, I wrote about research into how phages (viruses that kill bacteria) can understand the language of bacteria, allowing them to spy on their fellow gut inhabitants, thereby optimizing their own existence.  Discoveries into inter-species communication is pretty new and revolutionary, and I am sure in the not-very-distant-future, will lead to whole new ways of treating gut and immune issues in humans.

Thus, I was extremely interested in an article[i] that I spotted a couple of days ago.  It was just published in the journal Cell – another prominent medical journal.  It sounds to me like a major breakthrough in understanding the answer the question:  “How do microbiome alterations make us sick?”

Over and over, I have written  – and posted articles on my Facebook page –  about how this and that illness (Parkinson’s, Alzheimer’s, diabetes, etc.) are all now known to be associated with bacterial microbiome alterations.  What the mechanism of action is though, and why some people develop one illness versus another, are completely unknown.

Which brings me back to today’s article…

Nitric oxide is a major communication molecule in the mammalian body, and thus, the body tightly regulates the amount of it.  It can attach to thousands of proteins in the body (the process is called S-nitrosylation), and in doing so, it can turn genes on and off.  Disruptions in this system are, “…broadly implicated in diseases such as Alzheimer’s, Parkinson’s, asthma, diabetes, heart disease, and cancer.”

It turns out that gut bacteria also produce nitric oxide and can use it to communicate with their host:  “…The new findings are akin to uncovering a chemical language common across species…”

The researchers fed developing worms, C.elegens (which are commonly used as a mammalian model), gut bacteria that produce nitric oxide. They then isolated a protein (ALG-1) that is prevalent in both the worms and humans, and is known to turn off certain genes, including ones critical for normal development.  The nitric oxide secreted by the bacteria attached to the ALG-1, and the worms then developed abnormally and died. “Too much nitric oxide from bacteria commanded the worms’ DNA silencing proteins and impaired healthy development.”

That is, too many nitric oxide producing bacteria can cause disease or developmental issues by changing the expression of genes in the body. Thus, it is conceivable that using probiotics, we can soon improve nitric oxide signaling to improve health:  “…the microbiota can shape the post-translational landscape of the host proteome to regulate microRNA activity, gene expression, and host development. Our findings suggest a general mechanism by which the microbiota may control host cellular functions, as well as a new role for gasotransmitters.”[ii]

Now how is THAT for a new vocabulary word for all of us:  gasotransmitters?  I looked it up: it is defined as, “Any simple, gaseous compound, synthesized by an organism, that has a biochemical function”[iii]  We knew our gut bugs were talking to our body.  Now we have an actual mechanism (at least the first one) for how they do so.

Of course, as always, more research needs to be done.  Still, looking at the pathways that bacteria use to communicate with their hosts is likely to become a huge field of research.  It’s exciting to think about the future, wherein, specifically tailored probiotic blends can be created to manipulate someone’s microbiome to address their health issues and risks!

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[i] https://www.eurekalert.org/pub_releases/2019-02/cwru-nc022119.php

[ii] Puneet, S., et al. “Regulation of microRNA machinery and development by interspecies s-nitrosylation.” Cell. DOI: 10.1016/j.cell.2019.01.037

[iii] https://www.yourdictionary.com/gasotransmitter

One Comment on “How Do the Microbiota Communicate with Their Host? Scientists Have Cracked the First Mechanism!

  1. Pingback: Food Allergy, the Microbiome and Epigenetics – THE BIOME BUZZ

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