Antidepressants, such as Prozac, are used regularly to treat mental health issues, but recent research suggests that they can also protect against major infections and life-threatening sepsis. Scientists at the Salk Institute have now discovered how drugs regulate the immune system and prevent infectious disease, providing insight that can give birth to a new generation of life-saving remedies and future pandemics Global readiness can be improved.
Salk study follows recent findings that users of selective serotonin Reppetech inhibitors (SSRIs) were less severe covid -19 infections like prozac and less likely to develop long covids. ,
Fluoxetine’s dual role in infection defense
Another study found that also known as Prosecac-Fluoxetin-was effective in protecting mice against sepisis, a life-drew condition in which the body’s immune system goes ahead for an infection and multiple -Ang’s failure or even death can cause death. By identifying a mechanism to explain the stunning defense-bursting effects of fluoxetine, Salk researchers have brought fluoxetine close to clinical testing and potentially other SSRIs for use against infection and immune disorders.
“When treating an infection, the optimal treatment strategy will be the one that kills bacteria or virus protecting our tissues and organs,” says Professor Genel Arace, the holder of the Salk Institute Legacy Chair and Huzzes Medical Institute. “Most of the medicines we have in our toolbox kill pathogens, but we were thrilled to know that fluoxetine can protect tissues and organs. It is essentially playing crime and defense, which is ideal, and especially one It is exciting to see in the medicine that we already know to use in humans.
While our immune system tries his best to protect us from infections, sometimes they can overract. In sepsis, inflammatory reaction is out of control that it begins to harm a person’s own tissues and organs at the point of failure. It is also characteristic of the same overrition of severe Kovid -19 disease.
A clear solution will probably be to suppress the inflammatory response, but doing so can actually make patients more vulnerable to their initial infection-and susceptible to new ones. Timing is also important, because immunospressive drugs need to be administered before any tissue damage.
Instead, an ideal treatment 1) will continuously control the intensity and duration of the immune response to prevent any physical damage and puts the body at risk to kill the infection.
How fluoxetin works against infection
To understand what SSRIs are doing in this context, researchers studied mice with bacterial infections and separated them into two categories: a fluoxetine pretended with a fluxetion and not the other. Exciting, he saw that mice with fluoxetin were protected from sepsis, multi-organs damage and death. The team then launched a series of follow -up experiments to create an understanding of these effects.
First, he measured the number of bacteria in each mouse population eight hours after the infection. Rats treated with fluoxetine had low bacteria at this level, indicating less severe infections. Conclusions showed that fluoxetine had anti -antimicrobial properties, which allowed it to limit bacteria.
Next, researchers measured the levels of various inflammatory molecules in each group. He looked at the more anti-inflammatory IL-10 in his pretense population and reduced that IL-10 prevented sepsis-inspired hypertriglycridemia-a condition that contains too much fatty triglycerides in the blood. This enabled the heart to maintain proper metabolic state, protecting mice from transition-inspired sickness and mortality.
The team removed this IL-10-dependent security from its earlier discovery of Phulaveen’s antimicrobial effects from death due to multi-face damage and death, in return, killing the dual-staple ability of the drug 1) and 2) reduces infection-induced damage. Body.
Future research and potential clinical application
To understand how the effects of fluoxetin at the level of serotonin can contribute to these effects, researchers also saw two new mouse population: Both were pretended with fluoxetine, but one was broadcast serotonin. , While the other was not. Circulating serotonin is a small chemical messenger that travels to your brain and body to regulate things such as mood, sleep and pain, and the main goal for mental health effects of fluoxetine. He found that the positive health results of fluoxetine were completely unrelated to transmit serotonin-despite whether serotonin was in circulation in mice, he experienced similar infection defense benefits from fluoxetin.
“It was really unexpected, but also really exciting,” the first writer Robert Galant says, who is a former graduate student researcher in Ayres Lab. “Knowing fluxetion can regulate the immune response, protect the body from infection, and an antimicrobial effect-all are completely free from circulating serotonin-new solutions for life-threatening infections and diseases develop There is a big step towards doing it.
Ayres and Vallant say that their next step is to detect fluoxetin dodging regimens suitable for septic individuals. They are also curious to see if other SSRI can have the same effects.
“Fluoxetine, one of the most prescribed drugs in the United States, is promoting cooperation between hosts and pathogen to prevent transition-induced disease and mortality,” molecular and system called the major iers of physiology laboratories. “Finding dual protective and defensive effects in a renovated drug is really exciting.”
