We found that the incubation of MSCs with TNF-α and IFN-γ aggravates colitis, where high levels of pro-inflammatory factors, such as interleukin (IL)-17, IL-8, IL-12, IL-1β, transforming growth factor (TGF)-β, TNF-α and IFN-γ, were secreted.
Here, we use RNA interference to target CXCL8 and its receptor, CXCR1, to establish the existence of a functional signaling pathway promoting tumor growth initiated by sporadic and colitis CCSCs.
MIR301A-knockout mice were resistant to the development of colitis following administration of DSS; their colon tissues expressed lower levels of interleukin 1β (IL1β), IL6, IL8, and tumor necrosis factor than colons of control mice.
IL-8 was strongly up-regulated on systemic or local inflammatory stimulation, increasing mobilization of immature CD11b(+)Gr-1(+) myeloid cells (IMCs) with thioglycolate-induced peritonitis, DSS-induced colitis, and H. felis-induced gastritis.
The results suggest that GFW ameliorates colon inflammation by suppressing production of TNF-alpha as well as its signaling through NF-kappaB leading to the expression of inflammatory chemokines, MCP-1 and IL-8.
CM-induced tube formation and IL-8 production.Furthermore, B.P. facilitated recovery of mice from colitis as shown by increased body weight and reduced rectal bleeding and histological severity.B.P. also increased angiogenesis and mouse IL-8 production in the mucosal layer.