Asthma is an illness that affects 235 million people worldwide. It results in the involuntary narrowing of the trachea, along with an overproduction of mucus. Other symptoms of asthma are difficulty breathing, chest pain, along with coughing and gasping for air. Asthma attacks kill 250,000 individuals each year, and are intensified by airborne or food-borne pollutants and allergens. Asthma cannot be cured, however treatments, like prescription medication and inhalers, can use anti-inflammatory steroids and drugs that open up airways.

Thankfully, there is promising research that is being conducted by the Howard Hughes Medical Institute in Virginia suggesting that the nervous system has a large role to play in the study and treatment of asthma:

1. Sensory neurons
Various triggers of asthma have been studied to learn exactly what is happening inside the body when an asthma attack occurs. It has been known that the immune system plays a key role, as asthma is often triggered by an over-active response to any invaders in the body. Because of this, steroidal anti-inflammatory drugs are used to suppress the immune system. However, these drugs only work so well, leading researchers to believe there is another element at play. There are sensory neurons that are part of the vagal ganglia behind the esophagus. These neurons, in concordance with the rest of the vagus nerve, can control respiratory actions like coughing, as well as other symptoms of asthma.

2. TRPV1 and the immune response
Mice who have been genetically altered to have an allergy to ovalbumin, a protein in egg whites, experience asthma-like symptoms when they are exposed. Using that to stimulate an asthma attack, it was discovered that mice who did not express symptoms all had inactive neurons in the vagal ganglia, specifically those that produced a cellular receptor called Transient Receptor Potential Vallinoid 1(TRPV1). Interestingly, the immune systems of these mice still reacted to the ovalbumin normally by creating antibodies and increased white blood cells in the lungs, however there was no asthmatic episode. Because of this, it has been suggested that the immune system creates neuron signaling chemicals as part of the allergic reaction, which then cause asthmatic symptoms.

3. S1P and sensory nerve stimulation
Those neuron signals have been discovered to be a chemical called sphingosine-1-phosphate, abbreviated as S1P. This signaling molecule was found in the lungs of mice allergic to ovalbumin, and thought to be related to the development of asthma. Mice injected with S1P experienced asthmatic symptoms of narrowed tracheas and difficulty breathing, except those without the neurons expressing TRPV1. This suggests that immune response and inflammation in the lungs can lead to the creation of neuron stimulating molecules like S1P that can lead to asthma symptoms and attacks.

4. New therapies
The current treatments for asthma are ones that focus on suppressing the immune response or force the trachea open, both of which can cause side effects that can exacerbate the problem. Using therapies that work with the nervous system by blocking the use of the TRPV1 receptor would allow the body to prevent asthma attacks without harming the immune system. And though TRPV1 is prevalent throughout the body, for this treatment to be effective, only the neurons located on the vagal ganglia would need to be impacted. While researchers are still piecing together the true connection between asthma and the nervous system, it has become evident that there is more to the disease than just an over-active immune response.