When we become infected with one of the viruses responsible for gripe we experience symptoms such as sore throat or headache, cough, fever, or runny nose, among others, and a new study has discovered how does our brain know that we have contracted the disease, a finding that represents a first step to better understand the connection between the brain and the rest of the body when an infection occurs.
The research has been carried out by scientists from the Harvard Medical School in mice and has found that a group of neurons present in the respiratory tract takes care of alert the brain that we have contracted the flu. They have also found signs of a second information pathway from the lungs to the brain that is activated later.
“This study helps us to begin to understand a basic mechanism of pathogen detection and how it relates to the nervous system, which until now has been largely mysterious,” said the lead author. Stephen LiberlesProfessor of Cell Biology at the Blavatnik Institute at HMS and a Howard Hughes Medical Institute Investigator, whose lab investigates how the body and brain communicate to control physiology.
“We think these neurons relay the information that a pathogen is there and initiate neural circuits that control the response to influenza.”
Liberles has explained that when an infection occurs, the brain organizes the symptoms as the body generates the immune responseand that can include fever, lethargy, lack of appetite, and other more specific ones such as nasal congestion or cough when it comes to a respiratory disease, or vomiting and diarrhea when it comes to a gastrointestinal infection.
New therapeutic targets to combat influenza
In the new research they focused on influenza and through experiments with mice Na-Ryum Bin, one of the HMS researchers in Liberles’ lab, identified a small population of neurons found in the glossopharyngeal nerve, which runs from the throat up to the brain The scientist discovered that these neurons are the ones that indicate to the brain that there is a flu infection and have receptors for lipids called prostaglandins. Both mice and humans produce these lipids during infection, and as such are the targets of drugs such as ibuprofen and the aspirin.
Experiments included cutting the glossopharyngeal nerve, removing neurons, blocking prostaglandin receptors on those neurons, or giving the mice ibuprofen, which similarly decreased flu symptoms and increased animal survival.
The findings have been published in Nature and suggest that these airway neurons detect prostaglandins produced during a flu infection and become a communication pathway from the upper throat to the brain. “We think that these neurons transmit the information that there is a pathogen there and initiate neural circuits that control the response to the disease,” Liberles said.
The results provide an explanation for how drugs such as ibuprofen and aspirin work to reduce flu symptoms, and suggest that these drugs may even increase survival. They also discovered another possible disease pathway that goes from the lungs to the brain and that would be activated in the second phase of the infection when the virus penetrates further into the respiratory system, but they observed that prostaglandins are not involved at this stage and that the mice do not They responded to ibuprofen.
If these findings can be reproduced in humans, they could help develop influenza treatments that alleviate infection both during the prostaglandin phase, and in this second route of infection. “If a way can be found to inhibit both pathways and use them in synergy, that would be incredibly exciting and potentially transformative,” concludes Liberles.
Source: www.webconsultas.com
