Mesenchymal stem/stromal cells primed by inflammatory cytokines alleviate psoriasis-like inflammation via the TSG-6-neutrophil axis.
Yayun DingPixia GongJunjie JiangChao FengYanan LiXiao SuXiaojing BaiChenchang XuChunxiao LiuJianxin YangJiankai FangXiaocao JiYongjing ChenPeishan LiLingchuan GuoChangshun ShaoYufang ShiPublished in: Cell death & disease (2022)
Psoriasis is currently an incurable skin disorder mainly driven by a chronic inflammatory response. We found that subcutaneous application of umbilical cord- derived mesenchymal stem/stromal cells (MSCs) primed by IFN-γ and TNF-α, referred to as MSCs-IT, exhibited remarkable therapeutic efficacy on imiquimod (IMQ)-induced psoriasis-like inflammation in mice. Neutrophil infiltration, a hallmark of psoriasis, was significantly reduced after treatment with MSCs-IT. We further demonstrated that the effects of MSCs-IT were mediated by tumor necrosis factor (TNF) stimulating gene-6 (TSG-6), which was greatly upregulated in MSCs upon IFN-γ and TNF-α stimulation. MSCs transduced with TSG-6 siRNA lost their therapeutic efficacy while recombinant TSG-6 applied alone could also reduce neutrophil infiltration and alleviate the psoriatic lesions. Furthermore, we demonstrated that TSG-6 could inhibit neutrophil recruitment by decreasing the expression of CXCL1, which may be related to the reduced level of STAT1 phosphorylation in the keratinocytes. Thus, blocking neutrophil recruitment by MSCs-IT or TSG-6 has potential for therapeutic application in human psoriasis.
Keyphrases
- umbilical cord
- mesenchymal stem cells
- rheumatoid arthritis
- bone marrow
- inflammatory response
- oxidative stress
- stem cells
- atopic dermatitis
- immune response
- endothelial cells
- dendritic cells
- poor prognosis
- type diabetes
- cell proliferation
- genome wide
- disease activity
- systemic lupus erythematosus
- copy number
- drug delivery
- diabetic rats
- ankylosing spondylitis
- cancer therapy
- drug induced
- binding protein
- high fat diet induced
- wound healing
- stress induced
- transcription factor
- toll like receptor
- pluripotent stem cells