Researchers at the University of British Columbia have made a groundbreaking discovery about how the depletion of microbes in a newborn’s gut by antibiotics can lead to lifelong respiratory allergies. Published in the Journal of Allergy and Clinical Immunology, the study conducted by the school of biomedical engineering has identified a specific cascade of events that lead to allergies and asthma. This new insight has opened up numerous possibilities for exploring potential preventions and treatments for these conditions. Senior author Dr. Kelly McNagny explains that the research demonstrates how gut bacteria and antibiotics shape a newborn’s immune system, making them more prone to allergies, and highlights the long-lasting consequences on susceptibility to chronic diseases.
Allergies occur when the immune system reacts too strongly to harmless substances, such as pollen or pet dander, leading to symptoms like sneezing, itching, or swelling. The immune system normally protects individuals from harmful invaders like bacteria, viruses, and parasites, but in the case of allergies, harmless substances are mistaken for threats, triggering an immune response. Research has shown that the development of the immune system is established early in life, with microbes in the infant gut playing a crucial role. Infants often receive antibiotics shortly after birth to combat infections, which can reduce certain bacteria that produce a compound called butyrate, essential for halting processes related to allergies.
Studies conducted by Dr. McNagny’s lab have previously shown that infants with fewer butyrate-producing bacteria are more susceptible to allergies, and offering butyrate as a supplement in early life can help mitigate or reverse this vulnerability. By studying the process in mice, researchers have discovered that mice with depleted gut bacteria and no butyrate supplements developed a higher number of a specific type of immune cell called ILC2s, which are implicated in allergy development. These cells produce molecules that trigger white blood cells to produce abundant antibodies, coating cells as a defense mechanism against foreign invaders and resulting in an immune system that is hyper-reactive to allergens.
Butyrate must be provided during a specific window after birth, a few months for humans and a few weeks for mice, to prevent the proliferation of ILC2s and subsequent events. If this opportunity is missed and ILC2s multiply, the cascade continues and remains with the individual for life. With this new understanding of the steps involved in allergy development, researchers now have multiple potential targets for interrupting the cascade, even after the supplementation window closes. By identifying increased levels of ILC2s, it is possible to detect when a patient is on the verge of developing lifelong allergies, offering the potential to target these cell types rather than relying solely on butyrate supplementation.
Dr. McNagny and Dr. Michael Hughes emphasize that treating allergies with antihistamines and inhalers alleviates symptoms but does not cure the disease. To achieve lasting progress, it is essential to target the cells and mechanisms responsible for creating a hypersensitive immune system. The new insights provided by this research offer hope for more effective, long-term solutions that address the root cause of allergies, potentially paving the way for better management or even prevention of these conditions in the future. This research represents a significant step towards a future where allergies can be managed more effectively, ultimately improving the quality of life for individuals affected by these chronic conditions.