The Biology Blogger

In the intestines, there lurk these bacteria that aid in the digestion of different foods. In essence, they are a particular type of bacteria that is in a mutualistic relationship. Called commensals, there are typically anywhere from 300-500 of these bacteria in the intestines. The interesting thing is that despite the fact that they are bacteria, the immune system does not attack them. They live in our intestines and aid in a health digestive tract which seems almost contradictory because of the word bacteria going with them.

But, what a team of scientists have found is that these commensals do a lot more than just aid in the health of the digestive tract. Because the immune system has to deal with all different types of bacteria, it can have a hard time determining the difference between a commensal and an actual pathogen. In certain autoimmune diseases such as Crohn’s, the immune system attacks these commensal bacteria. So, how is it that the immune system knows typically not to attack the commensal bacteria?

By means of a certain interaction between the commensal bacteria and particular T-cells in the intestines, these commensals are able to stay alive. By binding with the receptor called Toll-like receptors (TLR), the commensal bacteria are given a means of survival. But, this doesn’t explain how they are able to help the immune system in fighting against pathogens.

The answer is in the immune cells called Tregs. They recognize the commensal bacteria and by recognizing them, help the immune system direct their attention to harmful pathogens. But, because of the existence of these Tregs, the other T-cells are kept at bay which is, in essence, a ‘weaker’ immune system. When a pathogen comes along, though, the DNA of these bacteria binds with TLR9, a receptor on the immune cells. By this occuring, Tregs are kept limited and other T-cells can come into being.

Since this happens, the T-cells can then go and attack the pathogen. But, because the commensal’s ‘aided’ in the attack, the T-cells don’t attack them; instead, they focus on the pathogens. It’s like the saying: ‘my enemies enemy is my ally.’

This leaves a lot of opportunities for certain therapies in oral and autoimmune diseases. But, the real question I have is: are we going to begin leaving antibiotics and perhaps using bacteria against themselves? It would be interesting to see what other kind of therapies can come from the research gained from this experiment.

Source.

What do you get when you use antibiotics far too much for any old sickness?  Antibiotic resistant bacteria is what you get.  Why?  It’s very simple.  The bacteria learn how to defend against whatever that antibacteria is.  It’s the same for anything.  If you cough on me, I’m going to get sick.  When I get better, if someone with that exact same strand of sickness coughs on me, I won’t get sick.  I’ve grown immune to it.  The same happens for bacteria.  They get immune to what we use against them and then continue to wreck havoc.

For instance, methicillin-resistant Staphylococcus aureus (MRSA) is a super bug.  No longer can it be treated with beta-lactam antibiotics.  Sure, there are antibiotics to counter MRSA, but as bacteria get used to different treatments, they become more and more resistant.  Add the fact that bacteria reproduce like crazy and you get a very simple understanding on why we need to be worried about these resistances.  Fortunately, there is hope.

Rockefeller University scientists have found a way to target the gene in the bacteria that creates this resistance.  In essence, they made a drug that removed the gene’s ability to make the bacteria resistant.  By doing that, the bacteria can be destroyed.  Called Ceftobiprole, this drug was tesed against MRSA which kills more people in and out of hospitals than any of the other drug-resistant bacteria.  The results from this were phenomenal.  100% knock out of the bacteria.  Not 50%.  Not 99.9%.  All bacteria were knocked out.

But, this wouldn’t be an effective treatment if they didn’t try other bacteria as well.  So, the scientists tesed Ceftobiprole on VRSA which is another S. aureus strain that is resistant to vancomycin.  What they found was incredible.  Ceftobiprole knocked them out as well.  By knocking out the gene that allows the bacteria to adapt and become resistant, the antibiotic was able to do its job in destroying the bacteria.

This research is interesting…For so long, the way the game worked was we created an antibiotic, used it for a while, and then stopped using it because the bacteria had grown resistant.  In this case, the bacteria can’t grow resistant.  Therefore, we can see the scientists had played a different game than normal.  Instead of trying to find a way to destroy the bacteria, they found a way to stop its resistance.  Get rid of its defenses and it becomes even easier to destroy.

I think this can prove incredibly useful in a lot of bacterial infections.  I can’t think of any way that the bacteria can best this.  However, science shows that anything is possible and I know that these scientists will have to continue working to ensure that they stay one up on the bacteria.  In this game, scientists won.  Scientists 1 - Bacteria 0.

Source: Science Daily.