Early life treatment with vancomycin reduces diabetes incidence in NOD mice

Camilla Hartmann Friis Hansen

Early life treatment with vancomycin reduces diabetes incidence in NOD mice

Abstract

Type 1 diabetes (T1D) results from an uncontrolled T cell mediated destruction of the insulin-producing beta-cells in the pancreas. Causal factors include a combination of genetics, early life incidents and the food we eat. The involved adaptive immune response can be down regulated by a regulatory immune response and a fine-tuned balance between these immunological components is crucial for characteristics of the disease, such as severity, onset time and recovery.
The balance between the regulatory and the adaptive immune response is heavily influenced by early life bacterial stimulation. An interplay that is likely to represent a critical environmental component to diabetes induction. In a period after birth alterations of the early microbial colonization of the gut therefore can be expected to have an immense impact on diabetes progression later in life.
In this study neonate NOD mice were treated with the antibiotic vancomycin in four weeks from birth. Diabetes incidence and onset time were compared with a control group and we found that neonate vancomycin treatment attenuates T1D. By changing the gut flora composition in the beginning of life we also demonstrated a disruption of the mechanisms regulating intestinal immune homeostasis toward a proinflammatory mucosal environment.

Originalsprog	Engelsk
Publikationsdato	jun. 2011
Status	Udgivet - jun. 2011
Begivenhed	International Congress of Mucosal Immunology - Paris, Frankrig Varighed: 5 jul. 2011 → 9 jul. 2011 Konferencens nummer: 11

Konference

Konference	International Congress of Mucosal Immunology
Nummer	11
Land/Område	Frankrig
By	Paris
Periode	05/07/2011 → 09/07/2011

FN’s Verdensmål

Dette resultat bidrager til følgende verdensmål

Citationsformater

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title = "Early life treatment with vancomycin reduces diabetes incidence in NOD mice",

abstract = "Type 1 diabetes (T1D) results from an uncontrolled T cell mediated destruction of the insulin-producing beta-cells in the pancreas. Causal factors include a combination of genetics, early life incidents and the food we eat. The involved adaptive immune response can be down regulated by a regulatory immune response and a fine-tuned balance between these immunological components is crucial for characteristics of the disease, such as severity, onset time and recovery. The balance between the regulatory and the adaptive immune response is heavily influenced by early life bacterial stimulation. An interplay that is likely to represent a critical environmental component to diabetes induction. In a period after birth alterations of the early microbial colonization of the gut therefore can be expected to have an immense impact on diabetes progression later in life. In this study neonate NOD mice were treated with the antibiotic vancomycin in four weeks from birth. Diabetes incidence and onset time were compared with a control group and we found that neonate vancomycin treatment attenuates T1D. By changing the gut flora composition in the beginning of life we also demonstrated a disruption of the mechanisms regulating intestinal immune homeostasis toward a proinflammatory mucosal environment. ",

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T1 - Early life treatment with vancomycin reduces diabetes incidence in NOD mice

AU - Hansen, Camilla Hartmann Friis

N1 - Conference code: 11

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N2 - Type 1 diabetes (T1D) results from an uncontrolled T cell mediated destruction of the insulin-producing beta-cells in the pancreas. Causal factors include a combination of genetics, early life incidents and the food we eat. The involved adaptive immune response can be down regulated by a regulatory immune response and a fine-tuned balance between these immunological components is crucial for characteristics of the disease, such as severity, onset time and recovery. The balance between the regulatory and the adaptive immune response is heavily influenced by early life bacterial stimulation. An interplay that is likely to represent a critical environmental component to diabetes induction. In a period after birth alterations of the early microbial colonization of the gut therefore can be expected to have an immense impact on diabetes progression later in life. In this study neonate NOD mice were treated with the antibiotic vancomycin in four weeks from birth. Diabetes incidence and onset time were compared with a control group and we found that neonate vancomycin treatment attenuates T1D. By changing the gut flora composition in the beginning of life we also demonstrated a disruption of the mechanisms regulating intestinal immune homeostasis toward a proinflammatory mucosal environment.

AB - Type 1 diabetes (T1D) results from an uncontrolled T cell mediated destruction of the insulin-producing beta-cells in the pancreas. Causal factors include a combination of genetics, early life incidents and the food we eat. The involved adaptive immune response can be down regulated by a regulatory immune response and a fine-tuned balance between these immunological components is crucial for characteristics of the disease, such as severity, onset time and recovery. The balance between the regulatory and the adaptive immune response is heavily influenced by early life bacterial stimulation. An interplay that is likely to represent a critical environmental component to diabetes induction. In a period after birth alterations of the early microbial colonization of the gut therefore can be expected to have an immense impact on diabetes progression later in life. In this study neonate NOD mice were treated with the antibiotic vancomycin in four weeks from birth. Diabetes incidence and onset time were compared with a control group and we found that neonate vancomycin treatment attenuates T1D. By changing the gut flora composition in the beginning of life we also demonstrated a disruption of the mechanisms regulating intestinal immune homeostasis toward a proinflammatory mucosal environment.

M3 - Poster

T2 - International Congress of Mucosal Immunology

Y2 - 5 July 2011 through 9 July 2011

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