Stress and corticotropin releasing factor (CRF) promote necrotizing enterocolitis in a formula-fed neonatal rat model
| Autor: | Frans A. Kuypers, Ginger S. Withers, Wolfgang Stehr, Robert L. Bell, Aditi Bhargava |
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| Přispěvatelé: | Yildirim, Arda |
| Rok vydání: | 2021 |
| Předmět: |
Epidemiology
Corticotropin-Releasing Hormone Low Birth Weight and Health of the Newborn Immune Receptors Biochemistry Infant Mortality Medicine and Health Sciences Medicine Hypoxia Receptor Immune Response Toll-like Receptors Barrier function Pediatric Immune System Proteins Multidisciplinary medicine.diagnostic_test Physics Classical Mechanics Infant Formula medicine.anatomical_structure Physical Sciences Necrotizing enterocolitis Mechanical Stress Anatomy medicine.symptom hormones hormone substitutes and hormone antagonists Research Article Signal Transduction medicine.medical_specialty Histology General Science & Technology Science Physiological Immunology Inflammation Ileum Stress Immunofluorescence Signs and Symptoms Rare Diseases Enterocolitis Necrotizing Stress Physiological Preterm Internal medicine Animals Enterocolitis Animal business.industry Prevention Antagonist Biology and Life Sciences Proteins Neonates Cell Biology Hypoxia (medical) Perinatal Period - Conditions Originating in Perinatal Period Newborn medicine.disease digestive system diseases Gastrointestinal Tract Disease Models Animal Thermal Stresses Good Health and Well Being Endocrinology Animals Newborn Disease Models TLR4 Clinical Medicine Necrotizing business Digestive System Developmental Biology Hormone |
| Zdroj: | PloS one, vol 16, iss 6 PLoS ONE, Vol 16, Iss 6 (2021) PLoS ONE PLoS ONE, Vol 16, Iss 6, p e0246412 (2021) |
| DOI: | 10.1101/2021.01.20.427423 |
| Popis: | The etiology of necrotizing enterocolitis (NEC) is not known. Alterations in gut microbiome, mucosal barrier function, immune cell activation, and blood flow are characterized events in its development, with stress as a contributing factor. The hormone corticotropin-releasing factor (CRF) is a key mediator of stress responses and influences these aforementioned processes. CRF signaling is modulated by NEC’s main risk factors of prematurity and formula feeding. Using an established neonatal rat model of NEC, we tested hypotheses that: (i) increased CRF levels—as seen during stress—promote NEC in formula-fed newborn rats, and (ii) antagonism of CRF action ameliorates NEC. Newborn pups were formula-fed to initiate gut inflammation and randomized to: no stress, no stress with subcutaneous CRF administration, stress (acute hypoxia followed by cold exposure—NEC model), or stress after pretreatment with the CRF peptide antagonist Astressin. Dam-fed unstressed and stressed littermates served as controls. NEC incidence and severity in the terminal ileum were determined using a histologic scoring system. Changes in CRF, CRF receptor (CRFRs), and toll-like receptor 4 (TLR4) expression levels were determined by immunofluorescence and immunoblotting, respectively. Stress exposure in FF neonates resulted in 40.0% NEC incidence, whereas exogenous CRF administration resulted in 51.7% NEC incidence compared to 8.7% in FF non-stressed neonates (p |
| Databáze: | OpenAIRE |
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