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

  1. Author:
    Chen, Lili [ORCID]
    Strohmeier, Valentina
    He, Zhengxiang [ORCID]
    Deshpande, Madhura
    Catalan-Dibene, Jovani [ORCID]
    Durum,Scott
    Moran, Thomas M
    Kraus, Thomas
    Xiong, Huabao
    Faith, Jeremiah J [ORCID]
    Sodhi, Chhinder P
    Hackam, David J [ORCID]
    Lira, Sergio A [ORCID]
    Furtado, Glaucia C [ORCID]

  2. Author Address

    Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA., Faculty of Biology, University of Freiburg, Schaenzlestrasse 1, 79104, Freiburg, Germany., Center for Cancer Research, National Cancer Institute, Frederick, MD, 21702, USA., Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA., Center for Therapeutic Antibody Development, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA., Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA., Division of General Pediatric Surgery, Johns Hopkins University and Bloomberg Children 39;s Center, Johns Hopkins Hospital, Baltimore, MD, 21287, USA., Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA. sergio.lira@mssm.edu., Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA. glaucia.furtado@mssm.edu.,
    1. Year: 2019
    2. Date: Oct 04
    3. Epub Date: 2019 10 04
  2. Journal: Nature communications
    1. 10
    2. 1
    3. Pages: 4517
  4. Type of Article: Article
  5. Article Number: 4517
  6. ISSN: 2041-1723
  1. 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.

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External Sources

  1. View Full Text
  2. DOI: 10.1038/s41467-019-12540-8
  3. PMID: 31586069
  4. View record in Web of Science®
  5. WOS: 000489013700010
  6. PII : 10.1038/s41467-019-12540-8

Library Notes

  1. Fiscal Year: FY2019-2020
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