Kouroupis Dimitrios, Best Thomas M, Kaplan Lee D, Correa Diego, Griswold Anthony J
Department of Orthopedic Surgery, UHealth Sports Medicine Institute, University of Miami, Miller School of Medicine, Miami, FL 33146, USA.
Diabetes Research Institute and Cell Transplant Center, University of Miami, Miller School of Medicine, Miami, FL 33136, USA.
Bioengineering (Basel). 2021 Oct 29;8(11):166. doi: 10.3390/bioengineering8110166.
The pathogenesis and progression of knee inflammatory pathologies is modulated partly by residing macrophages in the infrapatellar fat pad (IFP), thus, macrophage polarization towards pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes is important in joint disease pathologies. Alteration of M1/M2 balance contributes to the initiation and progression of joint inflammation and can be potentially altered with mesenchymal stem cell (MSC) therapy. In an acute synovial/IFP inflammation rat model a single intra-articular injection of IFP-MSC was performed, having as controls (1) diseased rats not receiving IFP-MSC and (2) non-diseased rats. After 4 days, cell specific transcriptional profiling via single-cell RNA-sequencing was performed on isolated IFP tissue from each group. Eight transcriptomically distinct cell populations were identified within the IFP across all three treatment groups with a noted difference in the proportion of myeloid cells across the groups. Largely myeloid cells consisted of macrophages (>90%); one M1 sub-cluster highly expressing pro-inflammatory markers and two M2 sub-clusters with one of them expressing higher levels of canonical M2 markers. Notably, the diseased samples (11.9%) had the lowest proportion of cells expressing M2 markers relative to healthy (14.8%) and MSC treated (19.4%) samples. These results suggest a phenotypic polarization of IFP macrophages towards the pro-inflammatory M1 phenotype in an acute model of inflammation, which are alleviated by IFP-MSC therapy inducing a switch towards an alternate M2 status. Understanding the IFP cellular heterogeneity and associated transcriptional programs may offer insights into novel therapeutic strategies for disabling joint disease pathologies.
膝关节炎性病变的发病机制和进展部分受髌下脂肪垫(IFP)中驻留巨噬细胞的调节,因此,巨噬细胞向促炎(M1)或抗炎(M2)表型的极化在关节疾病病变中很重要。M1/M2平衡的改变会导致关节炎症的发生和进展,并且间充质干细胞(MSC)治疗可能会改变这种平衡。在急性滑膜/IFP炎症大鼠模型中,对IFP-MSC进行单次关节内注射,设置两组对照:(1)未接受IFP-MSC的患病大鼠和(2)未患病大鼠。4天后,通过单细胞RNA测序对每组分离的IFP组织进行细胞特异性转录谱分析。在所有三个治疗组的IFP中鉴定出八个转录组不同的细胞群,各组间髓样细胞比例存在显著差异。髓样细胞主要由巨噬细胞组成(>90%);一个M1亚群高表达促炎标志物,两个M2亚群,其中一个表达更高水平的典型M2标志物。值得注意的是,相对于健康样本(14.8%)和MSC治疗样本(19.4%),患病样本中表达M2标志物的细胞比例最低(11.9%)。这些结果表明,在急性炎症模型中,IFP巨噬细胞向促炎M1表型发生了表型极化,而IFP-MSC治疗可诱导其向另一种M2状态转变,从而缓解这种极化。了解IFP细胞异质性和相关转录程序可能为治疗关节疾病病变的新策略提供思路。