Niimi Kimie, Takahashi Eiki
Support Unit for Animal Resources Development, Research Resources Division, RIKEN Center for Brain Science, 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan.
Research Resources Division, RIKEN Center for Brain Science, 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan.
J Vet Med Sci. 2021 May 9;83(5):784-792. doi: 10.1292/jvms.20-0532. Epub 2021 Mar 18.
Wasting marmoset syndrome (WMS) is a serious disease in captive common marmoset (Callithrix jacchus) colonies. Because of the high mortality rates, elucidation of the underlying mechanisms is essential. In this study, we compared the histopathology, the number of each epithelial cell in the jejunum and colon, and the expression patterns of some molecular markers between healthy and WMS-affected marmosets. Atrophy of villi in the jejunum and mononuclear cell infiltration in the lamina propria were observed in the intestinal tract of WMS-affected marmosets. Although the numbers of transient amplifying cells and tuft cells were increased, the number of goblet cells was obviously decreased in the jejunum and colon of WMS-affected marmosets compared to healthy marmosets. In addition, the number of enterocytes in the jejunum was decreased in WMS animals. There was no apparent difference in the numbers of stem cells, enteroendocrine cells, or Paneth cells. The expression of β-catenin and Tcf7l2 was increased in WMS, and the co-existence of β-catenin and Tcf7l2/Cyclin D1 was observed around the crypts in WMS-affected marmosets. These findings suggest that cell proliferation continues, but cell differentiation is halted in the intestinal tract due to the enhanced β-catenin/Tcf7l2/Cyclin D1signaling pathway in WMS, which results in malfunction of the villus and mucosa.
消瘦狨猴综合征（WMS）是圈养普通狨猴（Callithrix jacchus）群体中的一种严重疾病。由于死亡率高，阐明其潜在机制至关重要。在本研究中，我们比较了健康狨猴和受WMS影响的狨猴之间的组织病理学、空肠和结肠中每种上皮细胞的数量以及一些分子标记的表达模式。在受WMS影响的狨猴肠道中观察到空肠绒毛萎缩和固有层单核细胞浸润。与健康狨猴相比，受WMS影响的狨猴空肠和结肠中短暂增殖细胞和簇状细胞的数量增加，而杯状细胞的数量明显减少。此外，WMS动物空肠中的肠上皮细胞数量减少。干细胞、肠内分泌细胞或潘氏细胞的数量没有明显差异。WMS中β-连环蛋白和Tcf7l2的表达增加，在受WMS影响的狨猴隐窝周围观察到β-连环蛋白与Tcf7l2/细胞周期蛋白D1共存。这些发现表明，由于WMS中β-连环蛋白/Tcf7l2/细胞周期蛋白D1信号通路增强，肠道中细胞增殖持续，但细胞分化停止，导致绒毛和黏膜功能失调。
