Diabetes progression and alterations in ...
Type de document :
Article dans une revue scientifique: Article original
PMID :
URL permanente :
Titre :
Diabetes progression and alterations in gut bacterial translocation: prevention by diet supplementation with human milk in NOD mice.
Auteur(s) :
Sane, Famara [Auteur]
Laboratoire de virologie - ULR 3610
Scuotto, Angelo [Auteur]
Pierrat, Véronique [Auteur]
Hôpital Jeanne de Flandre [Lille]
Kacet, Nadine [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Hober, Didier [Auteur]
Laboratoire de virologie - ULR 3610
Romond, Marie-Benedicte [Auteur]
Laboratoire de virologie - ULR 3610
![refId](/themes/Mirage2//images/idref.png)
Laboratoire de virologie - ULR 3610
Scuotto, Angelo [Auteur]
Pierrat, Véronique [Auteur]
Hôpital Jeanne de Flandre [Lille]
Kacet, Nadine [Auteur]
Centre Hospitalier Régional Universitaire [CHU Lille] [CHRU Lille]
Hober, Didier [Auteur]
![refId](/themes/Mirage2//images/idref.png)
Laboratoire de virologie - ULR 3610
Romond, Marie-Benedicte [Auteur]
![refId](/themes/Mirage2//images/idref.png)
Laboratoire de virologie - ULR 3610
Titre de la revue :
Journal of Nutritional Biochemistry
Nom court de la revue :
J. Nutr. Biochem.
Numéro :
62
Pagination :
108-122
Date de publication :
2018-10-13
ISSN :
1873-4847
Mot(s)-clé(s) en anglais :
Human milk
Type 1 diabetes
Bacterial translocation
NOD mice
Microbiota
Type 1 diabetes
Bacterial translocation
NOD mice
Microbiota
Discipline(s) HAL :
Sciences du Vivant [q-bio]
Résumé en anglais : [en]
Impaired intestinal barrier function occurs before type 1 diabetes (T1D) onset with a possible contribution of microbial translocation. Breastfeeding is associated with enhanced mucosal intestinal integrity and T1D protection. ...
Lire la suite >Impaired intestinal barrier function occurs before type 1 diabetes (T1D) onset with a possible contribution of microbial translocation. Breastfeeding is associated with enhanced mucosal intestinal integrity and T1D protection. Our aim was to study the potential of human milk (HM) to prevent diabetes onset and modulate the translocation of gut bacteria susceptible to breastfeeding or associated to diabetes onset. We show that HM intake can prevent T1D in nonobese diabetic mice independently of bifidobacteria colonization. Prior to diabetes onset, HM mice harbored splenic bacterial counts and plasma lipopolysaccharides level similar to control mice but exhibited a reduced expansion of Anaerotruncus sp. in pancreas and Lactobacillus johnsonii and Barnesiella in Peyer's patches (PP). Surprisingly, pancreas and PP bacterial expansion did not correlate with their own gut localization but with ileal Escherichia coli and cecal HM-susceptible bacteria (the promoted L. murinus and Bacteroides vulgatus, and the repressed B. fragilis and E. coli), respectively. Besides, higher colonic B. vulgatus counts induced by HM intake were associated with low islet infiltration and pancreatic E. coli expansion. On another hand, splenic dendritic cells (DCs) were identified as negative covariate of PP Barnesiella, suggesting a possible HM contribution to preserving splenic DCs through the reduction of Barnesiella translocation. Fecal B. vulgatus also negatively correlated with PP Barnesiella expansion, indicating that the mouse coprophagic behavior likely added to HM effect. Our findings provide evidence that HM has a multilevel impact and cooperates with some gut bacteria for controlling bacterial translocation at the earliest stage of insulitis.Lire moins >
Lire la suite >Impaired intestinal barrier function occurs before type 1 diabetes (T1D) onset with a possible contribution of microbial translocation. Breastfeeding is associated with enhanced mucosal intestinal integrity and T1D protection. Our aim was to study the potential of human milk (HM) to prevent diabetes onset and modulate the translocation of gut bacteria susceptible to breastfeeding or associated to diabetes onset. We show that HM intake can prevent T1D in nonobese diabetic mice independently of bifidobacteria colonization. Prior to diabetes onset, HM mice harbored splenic bacterial counts and plasma lipopolysaccharides level similar to control mice but exhibited a reduced expansion of Anaerotruncus sp. in pancreas and Lactobacillus johnsonii and Barnesiella in Peyer's patches (PP). Surprisingly, pancreas and PP bacterial expansion did not correlate with their own gut localization but with ileal Escherichia coli and cecal HM-susceptible bacteria (the promoted L. murinus and Bacteroides vulgatus, and the repressed B. fragilis and E. coli), respectively. Besides, higher colonic B. vulgatus counts induced by HM intake were associated with low islet infiltration and pancreatic E. coli expansion. On another hand, splenic dendritic cells (DCs) were identified as negative covariate of PP Barnesiella, suggesting a possible HM contribution to preserving splenic DCs through the reduction of Barnesiella translocation. Fecal B. vulgatus also negatively correlated with PP Barnesiella expansion, indicating that the mouse coprophagic behavior likely added to HM effect. Our findings provide evidence that HM has a multilevel impact and cooperates with some gut bacteria for controlling bacterial translocation at the earliest stage of insulitis.Lire moins >
Langue :
Anglais
Audience :
Internationale
Vulgarisation :
Non
Établissement(s) :
Université de Lille
CHU Lille
CHU Lille
Collections :
Date de dépôt :
2024-01-17T22:49:22Z
2024-02-09T13:40:15Z
2024-02-09T13:40:15Z