Experimental models developed in "clean" laboratory mice rarely translates to human diseases. For example, NOD mice spontaneously develop Type 1 diabetes, as susceptible humans do, however pancreatic tissue pathology does not match.
There is another model of T1D in mice called treptozotocin (STZ)-induced diabetes. STZ is toxic to insulin producing β cells in pancreas and drive T1D in a T cell-dependent manner. In new study published in Journal of Experimental Medicine the authors showed that treptozotocin induced T1D depended on gut flora derived muramyl dipeptide → NOD2 signaling.
The authors found that NOD2-/- mice, but not NOD1-/- or Rip2-/- mice, were resistant to STZ effect.
Interestingly, similar protective effect against T1D were seen in WT mice treated with broad-spectrum antibiotics and STZ. However, addition of NOD2 ligand muramyl dipeptide reversed protection in [antibiotic + STZ] treated mice.
This study showed that NOD2 ligand, muramyl dipeptide derived from gut microbiota, contributes to T1D in STZ-treated mice.
David Usharauli
The authors found that NOD2-/- mice, but not NOD1-/- or Rip2-/- mice, were resistant to STZ effect.
Interestingly, similar protective effect against T1D were seen in WT mice treated with broad-spectrum antibiotics and STZ. However, addition of NOD2 ligand muramyl dipeptide reversed protection in [antibiotic + STZ] treated mice.
This study showed that NOD2 ligand, muramyl dipeptide derived from gut microbiota, contributes to T1D in STZ-treated mice.
David Usharauli
Hi great reading your bllog
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