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Interleukin 22 disrupts pancreatic function in newborn mice expressing IL-23
Lili Chen1, Valentina Strohmeier1,2, Zhengxiang He1
1Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.
Nature Communications
|October 6, 2019
Summary
Elevated IL-23 and IL-22 in newborns cause inflammation and poor nutrient absorption by impairing pancreatic enzyme production. Restoring IL-22 levels improves growth in affected neonate mice.
Area of Science:
- Immunology
- Gastroenterology
- Developmental Biology
Background:
- Neonatal inflammatory diseases lead to significant morbidity.
- The specific inflammatory factors and mechanisms driving these conditions remain unclear.
Purpose of the Study:
- To investigate the role of IL-23 and IL-22 in neonatal necrotizing enterocolitis.
- To elucidate the mechanisms by which these cytokines affect pancreatic function and nutrient absorption.
Main Methods:
- Neonatal mice models with elevated IL-23/IL-22 were studied.
- Gene expression analysis of intestinal and pancreatic enzymes was performed.
- The impact of germ-free conditions and IL-22 genetic ablation was assessed.
Main Results:
- Overexpression of IL-23/IL-22 in neonate mice led to systemic inflammation, nutrient malabsorption, and reduced pancreatic enzyme production.
- These mice exhibited decreased expression of genes essential for digestion and absorption.
- Germ-free environments improved outcomes, and genetic removal of IL-22 normalized growth in IL-23 overexpressing mice.
Conclusions:
- Increased IL-23 and IL-22 during early life negatively impacts pancreatic enzyme secretion and intestinal nutrient absorption.
- IL-22 directly reduces pancreatic acinar cell expression of PTF1a, a key transcription factor for pancreatic development.
