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Early growth restriction disrupts mice intestinal clock and homeostasis without being prevented by lactoferrin
Léa Chantal Tran1,2, Lucie Marousez3, Edwina Micours3
1Univ. Lille, Inserm, CHU Lille, U1286-INFINITE-Institute for Translational Research in Inflammation, Lille, France. lea.tran@chu-lille.fr.
Insights
Postnatal growth restriction impacts intestinal development and gene expression. Bovine lactoferrin supplementation did not improve growth but modulated gut microbiota in control pups, offering potential benefits for gut health.
Area of Science:
- Gastroenterology
- Developmental Biology
- Microbiology
Background:
- Preterm infants and growth-restricted newborns are vulnerable to intestinal inflammation and sepsis.
- Postnatal growth restriction (PNGR) affects intestinal development and immune responses.
- Bovine lactoferrin (bLf) is explored for its potential therapeutic effects.
Purpose of the Study:
- To investigate the effects of oral bovine lactoferrin (bLf) supplementation on intestinal development in postnatal growth-restricted (PNGR) mice.
- To assess the impact of PNGR and bLf on susceptibility to colitis at weaning.
- To analyze changes in intestinal transcriptome, microbiota, and short-chain fatty acids.
Main Methods:
- Growth restriction induced in mice from postnatal day 4 to 21.
- bLf administered from postnatal day 8 to 21.
- Intestinal function assessed via morphology, RNA sequencing, microbiota, and SCFA levels; colitis induced with DSS at postnatal day 22.
Main Results:
- PNGR altered intestinal gene expression related to circadian rhythm but did not increase colitis susceptibility post-weaning.
- bLf supplementation did not improve PNGR-induced growth retardation or intestinal immaturity.
- bLf affected microbiota in control pups and slightly reduced colitis inflammation in PNGR pups.
Conclusions:
- PNGR alters intestinal development through transcriptome changes during lactation.
- bLf supplementation does not reverse growth restriction effects on gut health.
- bLf may modulate gut microbiota, particularly in control pups during lactation.
Background:
Preterm infants and growth-restricted newborns are highly susceptible to intestinal inflammation and sepsis. We studied the effects of oral supplementation with bovine lactoferrin (bLf) during lactation in postnatal growth-restricted (PNGR) mice on intestinal development and susceptibility to colitis at weaning.
Methods:
Growth restriction was induced in FVB/NRj mice from large litters from postnatal day (PN) 4 to 21. bLf (300 mg/kg/d) was administered from PN8 to PN21. Intestinal function was evaluated at PN21 by morphology, RNA sequencing, microbiota composition, and cecal short chain fatty acid levels. At PN22, acute colitis was induced by 3% dextran sulfate sodium (DSS). Colitis severity was assessed at PN29 histologically and RT-qPCR.
Results:
PNGR altered the expression of genes related to circadian rhythm in intestines but did not increase susceptibility to DSS-induced acute colitis post weaning. PNGR-induced growth retardation and intestinal immaturity were not improved by bLf supplementation. bLf supplementation affected the microbiota composition in control, but not PNGR pups, and slightly reduced the inflammatory effects of colitis in PNGR.
Conclusion:
PNGR alters intestinal development by affecting the intestinal transcriptome during lactation. bLf supplementation does not prevent growth restriction effects on gut health but could modulate gut microbiota in control pups during this period.
Impact:
Postnatal growth restriction induces changes in the intestinal transcriptome with a disruption of clock-related gene expression. Postnatal growth restriction alters intestinal microbiota composition but does not amplify the response to an inflammatory-induced acute colitis after weaning. Bovine lactoferrin supplementation does not improve an induced growth restriction and its altered intestinal barrier structure. Bovine lactoferrin supplementation may induce positive intestinal microbial changes especially in control mice during lactation.
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