The flu and COVID-19 are changing behavior and physiological responses. Illness behavior is the nervous system’s response to infection, including reactions such as fever, lethargy, loss of appetite, nausea, headache and body aches, decreased mood and desire to communicate with others.
Decreased mood and desire to communicate are essential at the societal level: because patients tend to isolate themselves, they are less likely to infect their acquaintances.
The feeling of nausea is also a nervous system response, which can contribute to recovery in some infections. Loss of appetite may improve survival in certain bacterial infections. However, in viral infections, loss of appetite is harmful. Thus, glucose intake is harmful during bacterial sepsis, blood glucose will provide the bacteria with available fuel, but glucose protects neurons from damage during influenza infection and improves survival.
Scientists at Harvard Medical School (USA) found that changing the response of neurons makes it possible to reduce mortality from respiratory infections by reducing eating disorders.
Why Neurons Respond to The Flu
The hormone-like substance prostaglandins cause painful behavior. Prostaglandin E2 (PGE2) increases the sensitivity of pain receptors, increasing pain. Prostaglandin E2 can enter the brain by crossing the blood-brain barrier or be synthesized directly in the brain.
The presence of PGE2 is detected by prostaglandin receptors EP1-EP4. Some nausea reactions associated with fever are related to the activation of the EP3 receptor. The EP3 receptor is expressed in various brain areas, peripheral neurons, immune and other cells. Blockade of the EP3 receptor in the hypothalamus reduces febrile reactions.
Influenza infection raises prostaglandin E2 levels. In a mouse study, the administration of PGE2 reduced appetite in mice. When influenza-infected mice were given 1 mg/mL ibuprofen in their drinking water or injected with aspirin (20 mg/kg), PGE2 levels decreased, appetite, water intake and body weight were restored, and mobility and survival were improved.
Influenza triggers behavioral changes through the prostaglandin receptor EP3, expressed on branches of the vagus and glossopharyngeal nerves. The glossopharyngeal nerve detects the presence of a respiratory viral infection when elevated levels of prostaglandins activate the EP3 receptor. Next, the glossopharyngeal nerve transmits information to the brain, starting a program of painful behavior. The scientists found that blockade of the prostaglandin EP3 receptor reduced disease behavior and improved appetite and survival, similar to ibuprofen and aspirin. Conversely, activation of the EP3 receptor suppressed the appetite of mice.
Non-Steroidal Anti-Inflammatory Drugs Can Change The Response of Neurons
Altering neuronal response to respiratory infection may reduce mortality by suppressing painful changes in eating behavior.
The enzyme cyclooxygenase is required for the synthesis of prostaglandins. Non-steroidal anti-inflammatory drugs (NSAIDs) block cyclooxygenase, reducing prostaglandin synthesis and therefore reducing pain, inflammation, and fever.
By inhibiting the synthesis of prostaglandin E2, NSAIDs such as ibuprofen, paracetamol and aspirin reduce fever and normalize eating behavior, improving the course of respiratory viral infections. However, long-term use of NSAIDs increases the risk of gastric and duodenal ulcers.
Conclusion
Taking NSAIDs at an early stage of infection reverses flu-induced reductions in appetite and water intake. In the early stage of the disease, the virus is most prevalent in the upper respiratory tract, and glossopharyngeal nerve receptors record elevated levels of prostaglandins. NSAIDs lower prostaglandin levels by inhibiting the activation of prostaglandin receptors in the glossopharyngeal nerve.
The virus is more prevalent in the lower respiratory tract later in the disease, and the vagus nerve primarily innervates the lungs. The late stage of the illness activates a different neural pathway and is independent of prostaglandin E2 and its EP3 receptor.
Non-steroidal anti-inflammatory drugs are effective in the early stages of influenza infection. NSAIDs reduce fever, improve appetite, and make the illness milder.
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Reference
An airway-to-brain sensory pathway mediates influenza-induced sickness
