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Start Over Author "Elizabeth Huang" Journal cell reports medicine
2 results on '"Elizabeth Huang"'

1. Interleukin-22 signaling attenuates necrotizing enterocolitis by promoting epithelial cell regeneration

Author

Belgacem Mihi, Qingqing Gong, Lila S. Nolan, Sarah E. Gale, Martin Goree, Elise Hu, Wyatt E. Lanik, Jamie M. Rimer, Victoria Liu, Olivia B. Parks, Angela N. Lewis, Pranjal Agrawal, Marie L. Laury, Pawan Kumar, Elizabeth Huang, Shay S. Bidani, Cliff J. Luke, Jay K. Kolls, and Misty Good

Subjects
interleukin-22, necrotizing enterocolitis, epithelial cells, microbiome, regeneration, intestinal immunity, Medicine (General), R5-920
Abstract

Summary: Necrotizing enterocolitis (NEC) is a deadly intestinal inflammatory disorder that primarily affects premature infants and lacks adequate therapeutics. Interleukin (IL)-22 plays a critical role in gut barrier maintenance, promoting epithelial regeneration, and controlling intestinal inflammation in adult animal models. However, the importance of IL-22 signaling in neonates during NEC remains unknown. We investigated the role of IL-22 in the neonatal intestine under homeostatic and inflammatory conditions by using a mouse model of NEC. Our data reveal that Il22 expression in neonatal murine intestine is negligible until weaning, and both human and murine neonates lack IL-22 production during NEC. Mice deficient in IL-22 or lacking the IL-22 receptor in the intestine display a similar susceptibility to NEC, consistent with the lack of endogenous IL-22 during development. Strikingly, treatment with recombinant IL-22 during NEC substantially reduces inflammation and enhances epithelial regeneration. These findings may provide a new therapeutic strategy to attenuate NEC.

Published
2021
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2. Interleukin-22 signaling attenuates necrotizing enterocolitis by promoting epithelial cell regeneration

Author

Victoria Liu, Angela N. Lewis, Lila S. Nolan, Elizabeth Huang, Qingqing Gong, Misty Good, P. K. Agrawal, Martin Goree, Pawan Kumar, Olivia B. Parks, Jamie M. Rimer, Cliff J. Luke, Wyatt E. Lanik, Belgacem Mihi, Elise Hu, Sarah E. Gale, Shay S. Bidani, Jay K. Kolls, and Marie L. Laury

Subjects
Medicine (General), Chemokine CXCL1, Chemokine CXCL2, Interleukin-1beta, microbiome, Inflammation, Weaning, intestinal immunity, General Biochemistry, Genetics and Molecular Biology, Infant, Newborn, Diseases, Interleukin 22, Mice, R5-920, Enterocolitis, Necrotizing, Medicine, Animals, Humans, Protein Isoforms, Intestinal Mucosa, Receptor, Mice, Knockout, necrotizing enterocolitis, business.industry, Regeneration (biology), Interleukins, interleukin-22, Infant, Newborn, Interleukin, Gene Expression Regulation, Developmental, Receptors, Interleukin, medicine.disease, Preview, Epithelium, Recombinant Proteins, digestive system diseases, epithelial cells, Gastrointestinal Microbiome, Disease Models, Animal, medicine.anatomical_structure, Animals, Newborn, regeneration, Necrotizing enterocolitis, Immunology, medicine.symptom, business, Homeostasis, Infant, Premature, Signal Transduction
Abstract

Necrotizing enterocolitis (NEC) is an intestinal disorder that disproportionately affects premature infants and lacks in effective therapeutics. Mihi and colleagues1 demonstrated that the cytokine interleukin-22 promotes intestinal epithelial regeneration and reduces disease severity in an experimental model of NEC., Necrotizing enterocolitis (NEC) is an intestinal disorder that disproportionately affects premature infants and lacks in effective therapeutics. Mihi and colleagues demonstrated that the cytokine interleukin-22 promotes intestinal epithelial regeneration and reduces disease severity in an experimental model of NEC.

Published
2021

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