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Status: Completed.
This work was lead by my colleague Svenja Loering during her PhD, of which I am a co-author.
This work was lead by my colleague Svenja Loering during her PhD, of which I am a co-author.
This research project investigated the role of type 2 innate lymphoid cells (ILC2) in lung development and respiratory diseases. Lung development continues after birth, with significant remodelling in the first two weeks of a mouse's life. During this period, there was an increase in ILC2 and interleukin-33 (IL-33) in the lungs. Neonatal lung ILC2 were more abundant than those in adult lungs, suggesting a role in postnatal lung development. Early-life respiratory issues, such as those caused by premature birth or infections, could adversely affect lung development and increase the risk of chronic respiratory diseases like asthma and COPD.
The project characterised neonatal lung ILC2 in mice, examining their numbers, activation, and response to stimuli. It focused on the heterogeneity of lung ILC2, revealing differences in cell surface antigen expression, cytokine production, and responses based on age, sex, and mouse strain. The research explored the effects of altered ILC2 function on adult lung health, using ILC2-deficient mice and those with artificially increased ILC2. It found that early-life changes in ILC2 numbers and activation had persistent effects but didn't significantly alter adult lung structure or function.
The study also assessed how early-life ILC2 manipulation affected adult responses to respiratory diseases. Despite inducing lung pathology and inflammation, these changes appeared independent of early-life ILC2 alterations. The study concluded that while lung ILC2 are diverse and responsive to early-life stimuli, these changes don't significantly impact susceptibility to respiratory diseases in adulthood. Further research is needed to understand their role in lung development and disease.
The project characterised neonatal lung ILC2 in mice, examining their numbers, activation, and response to stimuli. It focused on the heterogeneity of lung ILC2, revealing differences in cell surface antigen expression, cytokine production, and responses based on age, sex, and mouse strain. The research explored the effects of altered ILC2 function on adult lung health, using ILC2-deficient mice and those with artificially increased ILC2. It found that early-life changes in ILC2 numbers and activation had persistent effects but didn't significantly alter adult lung structure or function.
The study also assessed how early-life ILC2 manipulation affected adult responses to respiratory diseases. Despite inducing lung pathology and inflammation, these changes appeared independent of early-life ILC2 alterations. The study concluded that while lung ILC2 are diverse and responsive to early-life stimuli, these changes don't significantly impact susceptibility to respiratory diseases in adulthood. Further research is needed to understand their role in lung development and disease.
