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Dextran sulphate sodium increases splenic Gr1+CD11b+ cells which accelerate recovery from colitis following intravenous transplantation
Summary 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 coliti...
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Published in: | Clinical and experimental immunology 2011-06, Vol.164 (3), p.417-427 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
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Online Access: | Get full text |
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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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ISSN: | 0009-9104 1365-2249 |
DOI: | 10.1111/j.1365-2249.2011.04374.x |