The team examined communication between the immune system and nervous system during inflammatory responses triggered by infections or allergens with helminths parasites to get a better understanding of how the body dampens immune responses. Exposure to these agents causes group 2 innate lymphoid immune cells to release inflammatory cytokine molecules which can promote increased mucus production and muscle contractions to help expel the agent from the body. However, prolonged or too much inflammation can be harmful.
Group 2 innate lymphoid immune cells have receptors on their surface called adrenergic receptors which interact with norepinephrine chemicals that the nerve cells release, these receptors give nerve cells the ability to interact with each other and the ability to influence immune responses. Model mice lacking in adrenergic receptors were exposed to helminths, which resulted in an exaggerated immune response to the infection and quicker expulsion of the parasites. Control mice treated with drugs to stimulate adrenergic receptors displayed an immune response that was blunted and helminth infection increased.
Beta-adrenergic receptors were found to control the proliferation of the group 2 innate lymphoid immune cells, the receptors may help to prevent too much inflammation, as noted by the researchers.
If researchers can successfully reproduce these promising results in humans it could have very important implications for patients suffering with inflammatory bowel disease, allergies, asthma, and other types of inflammatory diseases.
