Chronic intestinal inflammation alters hippocampal neurogenesis

• DOI: 10.1186/s12974-015-0281-0
• Publication Date: 2015-04-02T17:16:08Z
• Authors: Svetlana Zonis; Robert N Pechnick; Vladimir A Ljubimov; Michael Mahgerefteh; Kolja Wawrowsky; Kathrin S Michelsen; Vera Chesnokova
• Keywords: Doublecortin; Subgranular zone

Adult neurogenesis in the subgranular zone of hippocampus is involved learning, memory, and mood control. Decreased hippocampal elicits significant behavioral changes, including cognitive impairment depression. Inflammatory bowel disease (IBD) a group chronic inflammatory conditions intestinal tract, dysfunction depression frequently occur patients suffering from this disorder. We therefore tested effects inflammation on neurogenesis.The dextran sodium sulfate (DSS) mouse model IBD was used. Mice were treated with multiple-cycle administration 3% wt/vol DSS drinking water days 1 to 5, 8 12, 15 19, 22 26. sacrificed day 7 (acute phase inflammation) or 29 (chronic after beginning treatment.During acute inflammation, we found increased plasma levels IL-6 TNF-α expression Iba1, marker activated microglia, accompanied by induced IL-1β, cyclin-dependent kinase inhibitor p21(Cip1) (p21) hippocampus. During elevated. In hippocampus, p21 protein continued be induced. Furthermore, markers stem/early progenitor cells, nestin brain lipid binding (BLBP), neuronal doublecortin (DCX) all down-regulated, whereas glial fibrillary acidic (GFAP), for astroglia, addition, number proliferating precursors lineage assessed double Ki67 DCX staining significantly diminished DSS-treated animals, indicating decreased production new neurons.We show first time that alters neurogenesis. As arrests early proliferation, it likely induction during resulted reduction observed later, 29, treatment. The might underlie manifestations IBD.