Postnatal events in intestinal gene expression and splenic cell composition is altered in NOD mice

Publikation: KonferencebidragKonferenceabstrakt til konferenceForskningfagfællebedømt

Standard

Postnatal events in intestinal gene expression and splenic cell composition is altered in NOD mice. / Damlund, Dina Silke Malling; Metzdorff, Stine Broeng; Kristensen, Matilde Bylov; Hasselby, Jane Preuss; Hansen, Axel Jacob Kornerup; Buschard, Karsten; Frøkiær, Hanne.

2013. Abstract fra IDF 2013 World Diabetes Congress, Melbourne, Australien.

Publikation: KonferencebidragKonferenceabstrakt til konferenceForskningfagfællebedømt

Harvard

Damlund, DSM, Metzdorff, SB, Kristensen, MB, Hasselby, JP, Hansen, AJK, Buschard, K & Frøkiær, H 2013, 'Postnatal events in intestinal gene expression and splenic cell composition is altered in NOD mice', Melbourne, Australien, 02/12/2013 - 06/12/2013, .

APA

Damlund, D. S. M., Metzdorff, S. B., Kristensen, M. B., Hasselby, J. P., Hansen, A. J. K., Buschard, K., & Frøkiær, H. (2013). Postnatal events in intestinal gene expression and splenic cell composition is altered in NOD mice. Abstract fra IDF 2013 World Diabetes Congress, Melbourne, Australien.

Vancouver

Damlund DSM, Metzdorff SB, Kristensen MB, Hasselby JP, Hansen AJK, Buschard K o.a.. Postnatal events in intestinal gene expression and splenic cell composition is altered in NOD mice. 2013. Abstract fra IDF 2013 World Diabetes Congress, Melbourne, Australien.

Author

Damlund, Dina Silke Malling ; Metzdorff, Stine Broeng ; Kristensen, Matilde Bylov ; Hasselby, Jane Preuss ; Hansen, Axel Jacob Kornerup ; Buschard, Karsten ; Frøkiær, Hanne. / Postnatal events in intestinal gene expression and splenic cell composition is altered in NOD mice. Abstract fra IDF 2013 World Diabetes Congress, Melbourne, Australien.

Bibtex

@conference{eaeeac2f6c88409fa10551c8acbd0d85,
title = "Postnatal events in intestinal gene expression and splenic cell composition is altered in NOD mice",
abstract = "Evidence suggests that colonisation pattern of the gut in the early postnatal period is highly correlated with the risk of developing type 1 diabetes (T1D). We have recently shown that colonization in SPF mice accelerates gut maturation and that at postnatal day (PND) 1, in comparison with germ free mice, certain chemokines, including Cxcl2 encoding macrophage inflammatory protein (MIP)-2 and involved in attraction of neutrophils was downregulated in the gut epithelium. The non-obese diabetes (NOD) mouse is widely used as a model for studying the pathogenesis of T1D. The neonatal gut microbiota seems to play an important role in the development and control of T1D. We hypothesized that NOD mice in the perinatal period respond differently than mice not prone to develop T1D (C57/Bl6), and we investigated the differences in postnatal expression of genes in gut, spleen, liver and pancreas, cellular composition in spleen and liver.At PND1 and 2, the number of Ly-6G and CD11b positive cells in NOD mice was significantly (p=0.05) higher as compared to C57/bl6. Furthermore, gene expression analyses of liver, spleen and intestine showed differences between the two mouse strains in the early postnatal expression of Cxcl2 and the antibacterial lectin encoding RegIIIγ gene. Additionally histopathology findings of the liver showed significant differences of granulocyte infiltration between the two groups in the same period. Our findings suggest that very early postnatal microbiota dependent events contribute to the development of T1D in NOD mice.",
author = "Damlund, {Dina Silke Malling} and Metzdorff, {Stine Broeng} and Kristensen, {Matilde Bylov} and Hasselby, {Jane Preuss} and Hansen, {Axel Jacob Kornerup} and Karsten Buschard and Hanne Fr{\o}ki{\ae}r",
year = "2013",
month = "12",
language = "English",
note = "IDF 2013 World Diabetes Congress ; Conference date: 02-12-2013 Through 06-12-2013",

}

RIS

TY - ABST

T1 - Postnatal events in intestinal gene expression and splenic cell composition is altered in NOD mice

AU - Damlund, Dina Silke Malling

AU - Metzdorff, Stine Broeng

AU - Kristensen, Matilde Bylov

AU - Hasselby, Jane Preuss

AU - Hansen, Axel Jacob Kornerup

AU - Buschard, Karsten

AU - Frøkiær, Hanne

PY - 2013/12

Y1 - 2013/12

N2 - Evidence suggests that colonisation pattern of the gut in the early postnatal period is highly correlated with the risk of developing type 1 diabetes (T1D). We have recently shown that colonization in SPF mice accelerates gut maturation and that at postnatal day (PND) 1, in comparison with germ free mice, certain chemokines, including Cxcl2 encoding macrophage inflammatory protein (MIP)-2 and involved in attraction of neutrophils was downregulated in the gut epithelium. The non-obese diabetes (NOD) mouse is widely used as a model for studying the pathogenesis of T1D. The neonatal gut microbiota seems to play an important role in the development and control of T1D. We hypothesized that NOD mice in the perinatal period respond differently than mice not prone to develop T1D (C57/Bl6), and we investigated the differences in postnatal expression of genes in gut, spleen, liver and pancreas, cellular composition in spleen and liver.At PND1 and 2, the number of Ly-6G and CD11b positive cells in NOD mice was significantly (p=0.05) higher as compared to C57/bl6. Furthermore, gene expression analyses of liver, spleen and intestine showed differences between the two mouse strains in the early postnatal expression of Cxcl2 and the antibacterial lectin encoding RegIIIγ gene. Additionally histopathology findings of the liver showed significant differences of granulocyte infiltration between the two groups in the same period. Our findings suggest that very early postnatal microbiota dependent events contribute to the development of T1D in NOD mice.

AB - Evidence suggests that colonisation pattern of the gut in the early postnatal period is highly correlated with the risk of developing type 1 diabetes (T1D). We have recently shown that colonization in SPF mice accelerates gut maturation and that at postnatal day (PND) 1, in comparison with germ free mice, certain chemokines, including Cxcl2 encoding macrophage inflammatory protein (MIP)-2 and involved in attraction of neutrophils was downregulated in the gut epithelium. The non-obese diabetes (NOD) mouse is widely used as a model for studying the pathogenesis of T1D. The neonatal gut microbiota seems to play an important role in the development and control of T1D. We hypothesized that NOD mice in the perinatal period respond differently than mice not prone to develop T1D (C57/Bl6), and we investigated the differences in postnatal expression of genes in gut, spleen, liver and pancreas, cellular composition in spleen and liver.At PND1 and 2, the number of Ly-6G and CD11b positive cells in NOD mice was significantly (p=0.05) higher as compared to C57/bl6. Furthermore, gene expression analyses of liver, spleen and intestine showed differences between the two mouse strains in the early postnatal expression of Cxcl2 and the antibacterial lectin encoding RegIIIγ gene. Additionally histopathology findings of the liver showed significant differences of granulocyte infiltration between the two groups in the same period. Our findings suggest that very early postnatal microbiota dependent events contribute to the development of T1D in NOD mice.

M3 - Conference abstract for conference

ER -

ID: 213916797