Interleukin 22 disrupts pancreatic function in newborn mice expressing IL-23.

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ID: 57733
2019
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Abstract
Neonatal inflammatory diseases are associated with severe morbidity, but the inflammatory factors underlying them and their potential effector mechanisms are poorly defined. Here we show that necrotizing enterocolitis in neonate mice is accompanied by elevation of IL-23 and IL-22 and decreased production of pancreatic enzymes. These phenotypes are mirrored in neonate mice overexpressing IL-23 in CX3CR1 myeloid cells or in keratinocytes. The mice fail to grow and die prematurely, displaying systemic inflammation, nutrient malabsorption and decreased expression of intestinal and pancreatic genes mediating digestion and absorption of carbohydrates, proteins, and lipids. Germ-free environment improves, and genetic ablation of IL-22 restores normal growth in mice overexpressing IL-23. Mechanistically, IL-22 acts directly at the level of pancreatic acinar cells to decrease expression of the pancreas associated transcription factor 1a (PTF1a). These results show that augmented production of IL-23 and IL-22 in early life has a negative impact on pancreatic enzyme secretion and food absorption.
Reference Key
chen2019interleukinnature Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Chen, Lili;Strohmeier, Valentina;He, Zhengxiang;Deshpande, Madhura;Catalan-Dibene, Jovani;Durum, Scott K;Moran, Thomas M;Kraus, Thomas;Xiong, Huabao;Faith, Jeremiah J;Sodhi, Chhinder P;Hackam, David J;Lira, Sergio A;Furtado, Glaucia C;
Journal Nature communications
Year 2019
DOI
10.1038/s41467-019-12540-8
URL
Keywords
TNF-α inflammation viral load nfκb antibodies il-1β hhv-8 il-12

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