Amodeo, I. (Ilaria)

Filtering

2022 - 20232

Settings

Author search.filters.isAuthorOfPublication.024e7b2d-660e-46d9-ad9a-2d2ea6445883

Search Results

Now showing 1 - 2 of 2
  • Thumbnail Image
    Endothelial dysfunction in preterm infants: The hidden legacy of uteroplacental pathologies
    (Frontiers, 2022-11-04) Manzoni, F. (Francesca); Amodeo, I. (Ilaria); Gulden, S. (Silvia); Mosca, F. (Fabio); Provitera, L. (Livia); Tomaselli, A. (Andrea); Cavallaro, G. (Giacomo); Raffaeli, G. (Genny); Pravatà, V. (Valentina); Amelio, G.S. (Giacomo Simeone); Villamor, E. (Eduardo); Tripodi, M. (Matteo); Cortesi, V. (Valeria); Garrido-Martínez-de-Salazar, F. (Felipe); Cervellini, G. (Gaia)
    Millions of infants are born prematurely every year worldwide. Prematurity, particularly at lower gestational ages, is associated with high mortality and morbidity and is a significant global health burden. Pregnancy complications and preterm birth syndrome strongly impact neonatal clinical phenotypes and outcomes. The vascular endothelium is a pivotal regulator of fetal growth and development. In recent years, the key role of uteroplacental pathologies impairing endothelial homeostasis is emerging. Conditions leading to very and extremely preterm birth can be classified into two main pathophysiological patterns or endotypes: infection/inflammation and dysfunctional placentation. The first is frequently related to chorioamnionitis, whereas the second is commonly associated with hypertensive disorders of pregnancy and fetal growth restriction. The nature, timing, and extent of prenatal noxa may alter fetal and neonatal endothelial phenotype and functions. Changes in the luminal surface, oxidative stress, growth factors imbalance, and dysregulation of permeability and vascular tone are the leading causes of endothelial dysfunction in preterm infants. However, the available evidence regarding endothelial physiology and damage is limited in neonates compared to adults. Herein, we discuss the current knowledge on endothelial dysfunction in the infectious/inflammatory and dysfunctional placentation endotypes of prematurity, summarizing their molecular features, available biomarkers, and clinical impact. Furthermore, knowledge gaps, shadows, and future research perspectives are highlighted.
  • Thumbnail Image
    Human bone marrow-derived mesenchymal stromal cells reduce the severity of experimental necrotizing enterocolitis in a concentration-dependent manner
    (MDPI, 2023) Manzoni, F. (Francesca); Amodeo, I. (Ilaria); Gulden, S. (Silvia); Lonati, C. (Caterina); Mosca, F. (Fabio); Provitera, L. (Livia); Maggioni, M. (Marco); Tomaselli, A. (Andrea); Cerasani, J. (Jacopo); Cavallaro, G. (Giacomo); Pesenti, N. (Nicola); Raffaeli, G. (Genny); Crippa, S. (Stefania); Bernardo, M.E. (Maria Ester); Arribas-Sánchez, C. (Cristina); Amelio, G.S. (Giacomo Simeone); Oldoni, S. (Samanta); Menis, C. (Camilla); Tripodi, M. (Matteo); Cortesi, V. (Valeria); Santi, L. (Ludovica); Algieri, F. (Francesca); Garrido-Martínez-de-Salazar, F. (Felipe); Cervellini, G. (Gaia)
    : Necrotizing enterocolitis (NEC) is a devastating gut disease in preterm neonates. In NEC animal models, mesenchymal stromal cells (MSCs) administration has reduced the incidence and severity of NEC. We developed and characterized a novel mouse model of NEC to evaluate the effect of human bone marrow-derived MSCs (hBM-MSCs) in tissue regeneration and epithelial gut repair. NEC was induced in C57BL/6 mouse pups at postnatal days (PND) 3–6 by (A) gavage feeding term infant formula, (B) hypoxia/hypothermia, and (C) lipopolysaccharide. Intraperitoneal injections of PBS or two hBM-MSCs doses (0.5 × 106 or 1 × 106 ) were given on PND2. At PND 6, we harvested intestine samples from all groups. The NEC group showed an incidence of NEC of 50% compared with controls (p < 0.001). Severity of bowel damage was reduced by hBM-MSCs compared to the PBS-treated NEC group in a concentration-dependent manner, with hBM-MSCs (1 × 106 ) inducing a NEC incidence reduction of up to 0% (p < 0.001). We showed that hBM-MSCs enhanced intestinal cell survival, preserving intestinal barrier integrity and decreasing mucosal inflammation and apoptosis. In conclusion, we established a novel NEC animal model and demonstrated that hBM-MSCs administration reduced the NEC incidence and severity in a concentration-dependent manner, enhancing intestinal barrier integrity.