Vasoactive intestinal peptide decreases inflammation and tight junction disruption in experimental necrotizing enterocolitis.
Autor: | Seo S; Division of General and Thoracic Surgery, Translational Medicine Program, The Hospital for Sick Children, Toronto, Ontario, Canada; Department of Pediatric General and Urogenital Surgery, Juntendo University School of Medicine, Tokyo, Japan., Miyake H; Division of General and Thoracic Surgery, Translational Medicine Program, The Hospital for Sick Children, Toronto, Ontario, Canada; Department of Pediatric Surgery, Shizuoka Children's Hospital, Shizuoka, Japan., Alganabi M; Division of General and Thoracic Surgery, Translational Medicine Program, The Hospital for Sick Children, Toronto, Ontario, Canada., Janssen Lok M; Division of General and Thoracic Surgery, Translational Medicine Program, The Hospital for Sick Children, Toronto, Ontario, Canada., O'Connell JS; Division of General and Thoracic Surgery, Translational Medicine Program, The Hospital for Sick Children, Toronto, Ontario, Canada., Lee C; Division of General and Thoracic Surgery, Translational Medicine Program, The Hospital for Sick Children, Toronto, Ontario, Canada., Li B; Division of General and Thoracic Surgery, Translational Medicine Program, The Hospital for Sick Children, Toronto, Ontario, Canada., Pierro A; Division of General and Thoracic Surgery, Translational Medicine Program, The Hospital for Sick Children, Toronto, Ontario, Canada. Electronic address: agostino.pierro@sickkids.ca. |
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Jazyk: | angličtina |
Zdroj: | Journal of pediatric surgery [J Pediatr Surg] 2019 Dec; Vol. 54 (12), pp. 2520-2523. Date of Electronic Publication: 2019 Aug 30. |
DOI: | 10.1016/j.jpedsurg.2019.08.038 |
Abstrakt: | Background and Purpose: Excessive inflammatory cell infiltration and accumulation in the intestinal mucosa are pathological features of necrotizing enterocolitis (NEC) leading to intestinal barrier disruption. Vasoactive intestinal peptide (VIP) is a potent anti-inflammatory agent that regulates intestinal epithelial barrier homeostasis. We previously demonstrated that VIP-ergic neuron expression is decreased in experimental NEC ileum, and this may be associated with inflammation and barrier compromise. We hypothesize that exogenous VIP administration has a beneficial effect in NEC. Methods: NEC was induced in C57BL/6 mice by gavage feeding, hypoxia, and lipopolysaccharide administration between postnatal day (P) 5 and 9. There were four studied groups: Control (n = 6): Breast feeding without stress factors; Control + VIP (n = 5): Breast feeding + intraperitoneal VIP injection once a day from P5 to P9; NEC (n = 9): mice exposed to NEC induction; NEC + VIP (n = 9): NEC induction + intraperitoneal VIP injection. Terminal ileum was harvested on P9. NEC severity, intestinal inflammation, (IL-6 and TNFα), and Tight junctions (Claudin-3) were evaluated. Results: NEC severity and intestinal inflammation were significantly decreased in NEC + VIP compared to NEC. Tight junction expression was significantly increased in NEC + VIP compared to NEC. Conclusion: VIP administration has a beneficial therapeutic effect in NEC by reducing inflammation and tight junction disruption. (Copyright © 2019. Published by Elsevier Inc.) |
Databáze: | MEDLINE |
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