- Receptors present only on neurons associated with pruritus would be the cause of this disorder when it is chronic
- Knowledge of this mechanism could pave the way for new treatments
Itching – also called cutaneous pruritus – can be defined as a the uncomfortable feeling it causes should be scratched. They can be a symptom that accompanies a dermatological disease, such as eczema. This pathology, also called atopic dermatitis, affects genetically predisposed people. This severe itching is uncomfortable, chronic, sometimes incurable and can reduce the quality of life of patients. Researchers have just identified one of the mechanisms that may explain this cutaneous pruritus. Their work was published in a journal Proceedings of the National Academy of Sciences (PNAS). According to them, the amount of receptor for CysLT2 would be involved. A receptor is a structure present on a membrane or inside a cell. Its role is to receive messages that will modulate cellular activity.
The itching goes all the way to the brain
“Itching comes from a subset of neurons, and severe itching can be a protective response that will help us get rid of something that irritates the skin, says Chiu, co-author of the study. However, chronic itching is not protective and can be pathological. The underlying mechanism that activates neurons and causes chronic itching is not well understood and new treatment is needed.“Indeed, itching begins in the nerve endings located on the surface of the skin, at the level of specific receptors. This information is then transmitted to the sensory ganglia, to the spinal cord and eventually travels by nerve to the brain. Thus, it activates sensory, emotional and motor areas brain.
The cause of pruritus may be the presence of CysLT2R receptors
Therefore, the researchers wanted to identify the mechanisms that trigger this need for scratches in the context of chronic itching. To get their results, they analyzed the activity of sensory dorsal root ganglia – associated with itching in mice – that contain neurons. So, they noticed a significant amount CysLT2 receptors are present only on neurons associated with pruritus. After further experiments and research, they concluded that activation of these receptors induced a cutaneous pruritus in some mice with eczema, but not in all. This is because mice without CysLT2R receptors suffered less itching. The presence of CysLT2R receptors could therefore be the cause of itching and the possible development of eczema.
Towards new therapeutic pathways?
“The last ten years of research in the field of chronic pruritus have shown the importance and complexity of interactions between the immune system and the nervous system, emphasizes Tiphaine Voisin, lead author of the study. It was very exciting to investigate the contribution of leukotrienes.“The researchers continued their research by studying leukotrienes. They are mediators of inflammation, especially bronchial in the context of asthma. For the treatment of this pathology one of the proposed solutions is inhibition (c ‘, ie slowing or stopping) of leukotrienes, targeting CysLT1R receptors. to itch because it would be necessary to be able to target CysLT2R.However, currently no inhibitor has been scientifically validated to do so.The authors of the study therefore hope that future research will find this inhibitor that could offer new therapeutic pathways in the long run.So , once the nervous system is treated, the body’s immune response would work better and reduce the itching. “The immune system is much more complex than we think, says Frank Austen. Understanding nerve involvement is a huge step forward. It was the part that was missing in the study of inflammation. In my opinion, it is extremely important to connect neuroscience with those who study inflammation. ”