Multipotent adult progenitor cells prevent functional impairment and improve development in inflammation driven detriment of preterm ovine lungs

• DOI: 10.1016/j.reth.2024.03.014
• Publication Date: 2024-03-28T15:39:19Z
• Authors: Sophie M.L. Neuen; Daan R.M.G. Ophel...; Helene Widowski; Matthias C. Hütten; Tim Brokken; Charlotte van Gorp; Peter G.J. Nikkels; Carmen A.H. Sever...; Mireille M.J.P.E....; Clemens A. van Bl...; Freddy J. Troost; Vanessa L.S. LaPo...; Shahab Jolani; Christof Seiler; J. Jane Pillow; Tammo Delhaas; Niki L. Reynaert; Tim G.A.M. Wolfs
• Keywords: Bronchopulmonary Dysplasia

Perinatal inflammation increases the risk for bronchopulmonary dysplasia in preterm neonates, but underlying pathophysiological mechanisms remain largely unknown. Given their anti-inflammatory and regenerative capacity, multipotent adult progenitor cells (MAPC) are a promising cell-based therapy to prevent and/or treat negative pulmonary consequences of perinatal neonate. Therefore, pathophysiology adverse lung outcomes following benefits MAPC treatment at interface prenatal inflammatory postnatal ventilation exposures were elucidated. Instrumented ovine fetuses exposed intra-amniotic lipopolysaccharide (LPS 5 mg) 125 days gestation induce systemic peripheral organ outcomes. (10 × 106 cells) or saline administered intravenously two post LPS exposure. Fetuses delivered five either killed humanely immediately mechanically ventilated 72 h. Antenatal exposure resulted decreased alveolar maturation lung. Additionally, LPS-exposed lambs showed continued cell junction loss accompanied by edema, ultimately resulting higher oxygen demand. modulated inflammation, prevented epithelial endothelial barriers improved utero. These MAPC-driven improvements remained evident postnatally, concomitant edema functional loss. In conclusion, sensitizes underdeveloped subsequent injury, disturbed development impairment. partially prevents these changes is therefore approach infants