The incidence of type-1 diabetes in NOD mice is modulated by restricted flora not germ-free conditions

Cecile King, Nora E Sarvetnick

Research output: Contribution to journalArticle

94 Citations (Scopus)

Abstract

In the NOD mouse, the incidence of type-1 diabetes is thought to be influenced by the degree of cleanliness of the mouse colony. Studies collectively demonstrate that exposure to bacterial antigen or infection in the neonatal period prevents diabetes [1, 2, 3, 4, 5, 6, 7, 8, 9, 10], supporting the notion that immunostimulation can benefit the maturation of the postnatal immune system [11]. A widely accepted extrapolation from this data has been the notion that NOD mice maintained under germ-free conditions have an increased incidence of diabetes. However, evidence supporting this influential concept is surprisingly limited [12]. In this study, we demonstrate that the incidence of diabetes in female NOD mice remained unchanged under germ-free conditions. By contrast, a spontaneous monoculture with a gram-positive aerobic spore-forming rod delayed the onset and reduced the incidence of diabetes. These findings challenge the view that germ-free NOD mice have increased diabetes incidence and demonstrate that modulation of intestinal microbiota can prevent the development of type-1 diabetes.

Original languageEnglish (US)
Article numbere17049
JournalPloS one
Volume6
Issue number2
DOIs
StatePublished - Mar 7 2011

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Inbred NOD Mouse
insulin-dependent diabetes mellitus
Medical problems
Type 1 Diabetes Mellitus
diabetes
flora
incidence
Incidence
mice
bacterial antigens
Bacterial Antigens
bacterial infections
Spores
intestinal microorganisms
Bacterial Infections
immune system
Immune System
Immunization
Immune system
spores

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)
  • General

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The incidence of type-1 diabetes in NOD mice is modulated by restricted flora not germ-free conditions. / King, Cecile; Sarvetnick, Nora E.

In: PloS one, Vol. 6, No. 2, e17049, 07.03.2011.

Research output: Contribution to journalArticle

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