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For their own preservation, infectious bacteria often do their best to stay clear of our body’s immune system – and scientists have found a surreptitious and hitherto unknown way to do so.
What happens is that bacteria release toxins to disarm the mitochondria of immune cells, these tiny organelles that act like the engine rooms of cells. Once immune cells sense that their mitochondria are inactive, they trigger apoptosis or programmed cell death.
The results could give us new ways to fight infectious bacteria, especially those that have become resistant to antibiotics – although so far the experiments have only been conducted on mice in the lab.
“Ironically, it is the activation of host cell death factors that deals the final blow to mitochondria that induces apoptosis, not the bacterial toxins themselves,” explains molecular biologist Pankaj Deo of the Monash Biomedicine Discovery Institute (MBDI) in Australia.
In other words, bacterial toxins do not directly kill immune cells, but rather trigger a chain of events that cause our body’s emergency responders to kill themselves. Our immune cells use the mitochondria as sensors for infection.
This was the case with the mouse tests described in this study: by targeting the genetic controls of apoptosis in rodents, scientists were able to reduce inflammation in animals and decrease the risk of infection.
Bacterial pathogens Neisseria gonorrhoeaeuropathogenic Escherichia coli, and Pseudomonas aeruginosa were the ones that were tested – all of which are commonly found in hospitals and can develop drug resistance – but the team says the results would apply to other species of bacteria as well.
“We have shown in this article that we can speed up the immune response,” says molecular biologist Thomas Naderer of MBDI.
“The other aspect is if this response persists and we get constant inflammation – which is usually associated with bacterial infection and causes a lot of tissue damage – we have a new way to stop this tissue damaging inflammation. . “
Previously, attention had focused on bacterial toxins that created a different type of automatic cell death called pyroptosis. Here, the researchers spotted other toxins targeting mitochondria enveloped in structures called outer membrane vesicles.
Now that we know more about how mitochondria are targeted, maybe scientists could put a stop to it. More trials will be needed in humans to determine exactly what is going on with the microorganisms, but it is possible that existing drugs could be redesigned and new drugs developed to fight the infection.
With pathogens getting smarter and smarter when it comes to avoiding the drugs we send to defeat them – as well as evading the body’s own defenses – any new innovation in treatment could make a difference significant.
“There’s been a lot of effort trying to block endotoxins that kill immune cells, but this study really shifts the focus to different toxins that might be more important,” says Naderer. “This gives us some good leads that we can look at as a next step.”
The research was published in Microbiology of nature.
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