Abstract

Elucidating the mechanisms of bacterial translocation is crucial for the prevention and treatment of neonatal sepsis. In the present study, we aimed to evaluate the potential of lactoferrin to inhibit the development of late-onset blood infection in neonates. Our investigation evaluates the role of key stress factors leading to the translocation of intestinal bacteria into the bloodstream and, consequently, the development of life-threatening sepsis. Three stress factors, namely weaning, intraperitoneal administration of Gram-positive cocci and oral intake of Gram-negative rods, were found to act synergistically. We developed a novel model of rat pups sepsis induced by bacterial translocation and observed the inhibition of this process by supplementation of various forms of lactoferrin: iron-depleted (apolactoferrin), iron-saturated (hololactoferrin) and manganese-saturated lactoferrin. Additionally, lactoferrin saturated with manganese significantly increases the Lactobacillus bacterial population, which contributes to the fortification of the intestinal barrier and inhibits the translocation phenomenon. The acquired knowledge can be used to limit the development of sepsis in newborns in hospital neonatal intensive care units.

Highlights

  • Neonatal sepsis still represents an important cause of mortality and morbidity among infants [1]

  • Discussion we present the development of a novel animal model of neonatal sepsis induced by bacterial translocation and the application of such a model to elucidate the effect of oral supplementation with various forms of lactoferrin

  • We identified that lactoferrin saturated with manganese significantly increases the Lactobacillus bacterial population, which contributes to the fortification of the intestinal barrier and inhibits the translocation phenomenon

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Summary

Introduction

Neonatal sepsis still represents an important cause of mortality and morbidity among infants [1]. Onset sepsis appears up to 72 h after delivery and is usually associated with colonization by high-virulence etiological factors, from both the maternal vaginal (Streptococcus agalactiae and Streptococcus pyogenes) and gastrointestinal (GI) microbiota Late-onset sepsis is due to immature immunity including the skin, respiratory and gastrointestinal (GI) systems, need for invasive procedures, environmental exposures and prolonged hospital stay. In this case, positive blood cultures may be associated with both catheter-associated infection, nosocomial transmission and colonization factors [4]

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