Up-Regulation of Gr1+CD11b+ Population in Spleen of Dextran Sulfate Sodium Administered Mice Works to Repair Colitis

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.

IL-36R signalling activates intestinal epithelial cells and fibroblasts and promotes mucosal healing in vivo

“…In addition to IL-6, various chemokines guiding neutrophil recruitment were found among the most upregulated genes in our NGS studies addressing targets of IL-36R signalling in colonic fibroblasts. Although the role of neutrophils in experimental colitis und wound healing may be dependent on the molecular and cellular context, there is substantial evidence that they can contribute to a regenerative function upon intestinal mucosal damage 38 39. Moreover, deficiency in CXCL1 was connected with increased susceptibility to acute colitis40 which is in accordance with the observations in our work.…”

Gleaning Insights from Fecal Microbiota Transplantation and Probiotic Studies for the Rational Design of Combination Microbial Therapies

“…Neutrophils are important in wound healing and the maintenance of homeostatic processes through their phagocytosis of damaging cellular debris as well as through the secretion of growthpromoting factors such as vascular endothelial growth factor (VEGF), lipoxins, and protectins (257). Some studies have reported that depletion of Gr1 ϩ CD11b ϩ cells, including neutrophils, exacerbates mouse models of colitis, suggesting a protective role for neutrophils (260,261). However, other studies have demonstrated the opposite effect (262), perhaps due to differences in neutrophil depletion methods.…”

Up-regulation of Gr1+CD11b+ cell population in the spleen of NaClO-administered mice works to repair skin wounds

“…These results are correlated with our previous work, which showed upregulation of the GR-1 + CD11b + population in the spleen of DSS-treated mice. DSS also produces ROS in the intestine and induces neutrophil migration [18,19]. The transplantation of GR-1 + CD11b + cells in the early phase of wound healing induces early recovery of wound healing.…”

“…We have recently shown that Gr1 + CD11b + cells increased in the spleen of dextran sulphate sodium (DSS)-treated mice during the recovery phase and splenectomy worsened the colitis [18].…”