Abstract
Dextran sulfate sodium (DSS) is commonly used in rodent IBD models to chemically induce acute intestinal inflammation. The acute course of colitis includes colon tissue damages and recovery from wounded tissues. As skin wound repair was delayed by splenectomy, we asked whether splenectomy would induce the delay of colonic wound healing. In splenectomized mice, body weight recovery, disease score and colon length were delayed. Surprisingly we found a great increase of Gr1+CD11b+ cells in spleen and bone marrow of DSS-administered mice. Anti-Gr-1 antibody treatment worsened the DSS- administered colitis. These results indicate that Gr1+CD11b+ cells induced by DSS worked to repair colon wound healing and repair colitis.
Keywords: Ulcerative colitis, DSS, Gr-1, CD11b, myeloid-lineage, Inflammatory bowel disease (IBD), gastrointestinal, Crohn's disease, atherosclerosis, hypercholesterolemic, splenectomy, secreting antibodies, Dextran sulfate sodium (DSS), bloody diarrhea, epithelial cell damage, cell infiltration, oral administration, Biomedical, Colon Histology, epithelium, Disease Activity Index, gross bleeding, stool consistency, Immune Cells, myeloid cell, Lamina propria cells, Biosciences, thymus, bone marrow, Colon lengths, parasites, fungus, Trypanosoma cruzi infection, autoimmune, encephalomyelitis, high inflammatory monocytes
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