Emeritus Group Neuroimmunology

Gut Microbiota and spontaneous disease

Having distributed our transgenic RR mice to different laboratories, we noted strikingly different frequencies of spontaneous EAE in different housing facilities. One possible factor underlying this variation could be related to varied microbial environments. To directly study microbial factors responsible for the spontaneous EAE onset, we initially compared germ-free (GF) (devoid of intestinal flora) and conventionally raised mice (SPF) (regular intestinal flora) for occurrence of EAE and activation of T and B lymphocytes. We noted that, in contrast to mice housed in SPF conditions, GF transgenic mice were fully protected from spontaneous EAE (Fig. 3) (1).

<strong>Fig. 3.</strong> <strong>Intestinal microbiota is required for the development of spontaneous EAE.</strong> <strong>a</strong>, Incidence of spontaneous EAE in RR mice housed in germ-free (GF) or SPF conditions. <strong>b</strong>, Incidence of spontaneous EAE in germ-free RR mice re-colonized with conventional flora from SPF mice. Zoom Image
Fig. 3. Intestinal microbiota is required for the development of spontaneous EAE. a, Incidence of spontaneous EAE in RR mice housed in germ-free (GF) or SPF conditions. b, Incidence of spontaneous EAE in germ-free RR mice re-colonized with conventional flora from SPF mice. [less]

These findings open up an array of questions, which include: Does the commensal gut microbiota of MS patients differ from healthy people? Are there defined species of the gut microbiota that trigger or protect from spontaneous disease? Does diet contribute to the spontaneous autoimmune CNS disease?

Collaborators:

Prof. Dr. Rolf Kemler; Max Planck Institute of Immunobiology and Epigenetics, Molecular Embryology, Freiburg

Dr. Caroline Johner; Max Planck Institute of Immunobiology and Epigenetics, Freiburg

1. K. Berer et al., Nature 479, 538 (2011).

 
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