Unit:
Faculty of MedicineLibrary of the School of Health Sciences
Author:
Matara Dimitra-Ifigeneia
Dissertation committee:
Χρήστος Σαλάκος, Καθηγητής, Ιατρική Σχολή, ΕΚΠΑ
Θεόδωρος Ξάνθος, Καθηγητής, Τμήμα Μαιευτικής, ΠΑΔΑ
Μαρία Γαζούλη, Καθηγήτρια, Ιατρική Σχολή, ΕΚΠΑ
Νικολέττα Ιακωβίδου, Καθηγήτρια, Ιατρική Σχολή, ΕΚΠΑ
Ζωή Ηλιοδρομίτη, Αναπληρώτρια Καθηγήτρια, Ιατρική Σχολή, ΕΚΠΑ
Θεοδώρα Μπούτσικου, Αναπληρώτρια Καθηγήτρια, Ιατρική Σχολή, ΕΚΠΑ
Κωνσταντίνος Πανουλής, Καθηγητής, Ιατρική Σχολή, ΕΚΠΑ
Original Title:
Βακτηριακή διαμετάθεση σε μοντέλο ασφυξίας σε νεογνά χοιρίδια
Translated title:
Asphyxia-induced bacterial translocation in an animal experimental model in neonatal piglets
Summary:
Introduction and objectives
The term "bacterial translocation" (BT) refers to the migration of bacteria or their products from the gastrointestinal tract to tissues located outside it, and may occur after intestinal ischemia-reperfusion injury. The term "endotoxin" is synonymous, and is used interchangeably with the term lipopolysaccharide (LPS). LPS, a component of Gram-negative gut bacteria, is a potent microbial virulence factor, that can trigger production of pro-inflammatory mediators, causing localized and systemic inflammation. The aim of this study is to investigate if neonatal asphyxia provokes BT and an increased concentration of LPS in an animal model of asphyxia in piglets.
Methods
Twenty-one (21) newborn male Landrace/Large White piglets, 1-4 days old, were randomly allocated into three groups, Control (A), Asphyxia (B) and Asphyxia-Cardiopulmonary Resuscitation (CPR) (C). All animals were instrumented, anesthetized and underwent hemodynamic monitoring. In Group A, the animals were euthanized. In Group B, the endotracheal tube was occluded to cause asphyxia leading to cardiopulmonary arrest. In Group C, the animals were resuscitated after asphyxia and further monitored for 30'. Bacterial translocation was assessed by the measurement of endotoxin in blood from the portal vein and the aorta, and also by the measurement of endotoxin in mesenteric lymph nodes (MLNs) at euthanasia. The results are given as median (IQR) with LPS concentration in EU/mL.
Results
BT was observed in all groups with minimum LPS concentration in the MLN and maximum concentration in the portal vein. LPS levels in the MLNs were higher in the Group B: 6.38 EU/mL (2.69-9.34) compared to the other groups (Group A: 2.1 EU/mL (1.08-2.52), Group C: 1.66 EU/mL (1.51-2.48), p = 0.012). The aorta to MLNs LPS difference (%) was lower in Group B: 0.13% (0.04-1.17), compared to Group A: 5.08% (2.2-10.7), and Group C: 3.42% (1.5-5.1)) (p = 0.042). The same was detected for portal to MLNs LPS difference (%) which was lower in Group B: 0.94% (0.5-3) compared to Group A: 4.9% (4-15), and Group C: 3.85% (1.5-5.1)) (p = 0.044).
Conclusions
Neonatal asphyxia can provoke ΒΤ and increased LPS concentration in blood and tissue located outside the gastrointestinal system.
Main subject category:
Health Sciences
Keywords:
Animal model, Endotoxin, Gut microbiome, Intestinal ischemia, Lipopolysacharide, Microbial translocation, Neonatal asphyxia
Number of references:
364
File:
File access is restricted until 2026-12-29.
ΔΙΑΤΡΙΒΗ ΜΑΤΑΡΑ-FINAL- pergamos.pdf
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File access is restricted until 2026-12-29.
