While Gr1+CD11b+ cells are known to regulate immune responses and accumulate in most cancer tissues, the function of Gr1+CD11b+ cells in inflammation is poorly understood. We investigated the role of Gr1+CD11b+ cells in a dextran sulphate sodium (DSS)-treated mouse model of ulcerative colitis (UC). C57BL/6 mice were treated with 2% DSS in drinking water for 5 days. Disease progression and recovery were assessed by body weight, disease activity index score (DAI) score and colon length. Splenic Gr1+CD11b+ cell number was greatly increased during the recovery phase of DSS-induced colitis. DSS-derived splenic Gr1+CD11b+ cells were administered intravenously to recipient (C57BL/6) mice during the early phase of DSS treatment. The transplanted splenic DSS-induced Gr1+CD11b+ cells improved DSS-induced colitis and promoted efficient colonic mucosal healing. We found that the CD11b+ single positive cells increased in the course of DSS-induced colitis in lamina propria. The transplantation of splenic Gr1+CD11b+ cells induced feedback suppression of myeloid-lineage cell development. Namely, the transplantation of splenic Gr1+CD11b+ cells greatly suppressed the migration of CD11b+ single positive cells to the lamina propria. Further, transplantation of Gr-1+CD11b+ cells greatly suppressed the increase of the same population, especially during the late phase of DSS colitis both in spleen and bone marrow
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