Early life treatment with vancomycin reduces diabetes incidence in NOD mice

Research output: Contribution to conferencePosterResearch

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Early life treatment with vancomycin reduces diabetes incidence in NOD mice. / Hansen, Camilla Hartmann Friis; Nielsen, Dennis Sandris; Vogensen, Finn Kvist; Hansen, Axel Jacob Kornerup.

2011. Poster session presented at Mucosal Immunology and Health and Disease, San Fransisco, United States.

Research output: Contribution to conferencePosterResearch

Harvard

Hansen, CHF, Nielsen, DS, Vogensen, FK & Hansen, AJK 2011, 'Early life treatment with vancomycin reduces diabetes incidence in NOD mice', Mucosal Immunology and Health and Disease, San Fransisco, United States, 14/04/2011 - 16/04/2011.

APA

Hansen, C. H. F., Nielsen, D. S., Vogensen, F. K., & Hansen, A. J. K. (2011). Early life treatment with vancomycin reduces diabetes incidence in NOD mice. Poster session presented at Mucosal Immunology and Health and Disease, San Fransisco, United States.

Vancouver

Hansen CHF, Nielsen DS, Vogensen FK, Hansen AJK. Early life treatment with vancomycin reduces diabetes incidence in NOD mice. 2011. Poster session presented at Mucosal Immunology and Health and Disease, San Fransisco, United States.

Author

Hansen, Camilla Hartmann Friis ; Nielsen, Dennis Sandris ; Vogensen, Finn Kvist ; Hansen, Axel Jacob Kornerup. / Early life treatment with vancomycin reduces diabetes incidence in NOD mice. Poster session presented at Mucosal Immunology and Health and Disease, San Fransisco, United States.

Bibtex

@conference{aab869c783d740a8907cf2066d26a88c,
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.",
author = "Hansen, {Camilla Hartmann Friis} and Nielsen, {Dennis Sandris} and Vogensen, {Finn Kvist} and Hansen, {Axel Jacob Kornerup}",
year = "2011",
month = "4",
language = "English",
note = "null ; Conference date: 14-04-2011 Through 16-04-2011",

}

RIS

TY - CONF

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

AU - Hansen, Camilla Hartmann Friis

AU - Nielsen, Dennis Sandris

AU - Vogensen, Finn Kvist

AU - Hansen, Axel Jacob Kornerup

PY - 2011/4

Y1 - 2011/4

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

ER -

ID: 37812499