Mast cells that reside at different locations in the jejunum of mice infected with Trichinella spiralis exhibit sequential changes in their granule ultrastructure and chymase phenotype

Mast cells that reside at different locations in the jejunum of mice infected with Trichinella spiralis exhibit sequential changes in their granule ultrastructure and chymase phenotype
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DOI:
10.1083/jcb.135.1.279
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发表时间:
1996-10-01
影响因子:
7.8
通讯作者:
Stevens, RL
Stevens, RL
中科院分区:
生物学1区
文献类型:
--
作者:
Friend, DS;Ghildyal, N;Stevens, RL

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未转化的成熟小鼠肥大细胞(MC)或其定向祖细胞是否能在炎症反应中改变其颗粒蛋白酶表型,尚未确定。为了解决这个问题,颗粒形态和蛋白酶含量的MC在BALB/c小鼠暴露于旋毛虫感染过程中的空肠进行了评估。在1周内蠕虫感染的小鼠,MC的数量增加出现在隐窝在绒毛的基础上,并通过第2周的MC的数量增加了约25倍,整个绒毛。肥大细胞增多症高峰后不久,上皮内MC消失,随后固有层MC逐渐减少。在感染高峰期上皮内MC中存在含有晶体结构的星状颗粒,并且在肥大细胞增多症消退期间在固有层MC中保留具有碎片晶体的这种颗粒,这表明MC在炎症的各个阶段迁移。如通过连续切片的免疫组织化学分析所评估的,在表达小鼠MC蛋白酶(mMCP)5而不表达mMCP-1或mMCP-2的肌肉中以及在表达mMCP-1和mMCP-2而不表达mMCP-5的上皮中,在感染的高度观察到主要的糜酶表型。伴随着这两个MC人口的过渡形式在粘膜下层表达mMCP-2和mMCP-5没有mMCP-1和在固有层表达mMCP-2单独。这些数据表明,空肠MC依次表达mMCP-2,停止表达mMCP-5,并最终表达mMCP-1的细胞逐渐出现在粘膜下层,固有层,上皮细胞,分别。在疾病的恢复期,MC依次停止表达mMCP-1,表达mMCP-5,最后停止表达mMCP-2,因为它们分别存在于绒毛的顶端、绒毛的基部和粘膜下层。MC可以可逆地改变它们的蛋白酶表型,这表明具有固定功能含义的静态命名法不足以描述特定组织内炎症过程中的MC群体。
Whether or not a nontransformed, mature mouse mast cell (MC) or its committed progenitor can change its granule protease phenotype during inflammatory responses, has not been determined. To address this issue, the granule morphology and protease content of the MC in the jejunum of BALB/c mice exposed to Trichinella spiralis were assessed during the course of the infection. Within 1 wk after helminth infection of the mice, increased numbers of MC appeared in the crypts at the base of the villi, and by wk 2 the number of MC throughout the villi increased by similar to 25-fold. Shortly after the peak of the mastocytosis, the intraepithelial population of MC disappeared, followed by a progressive loss of lamina propria MC. The presence of stellate-shaped granules containing crystalline structures in intraepithelial MC at the height of infection and the retention of such granules with fragmented crystals in lamina propria MC during resolution of the mastocytosis suggest that MC migrate during the various phases of the inflammation. As assessed by immunohistochemical analyses of serial sections, predominant chymase phenotypes were observed at the height of the infection in the muscle that expressed mouse MC protease (mMCP) 5 without mMCP-1 or mMCP-2 and in the epithelium that expressed mMCP-1 and mMCP-2 without mMCP-5. Accompanying these two MC populations were transitional forms in the submucosa that expressed mMCP-2 and mMCP-5 without mMCP-1 and in the lamina propria that expressed mMCP-2 alone. These data suggest that jejunal MC sequentially express mMCP-2, cease expressing mMCP-5, and finally express mMCP-1 as the cells progressively appear in the submucosa, lamina propria, and epithelium, respectively. In the recovery phase of the disease, MC sequentially cease expressing mMCP-1, express mMCP-5, and finally cease expressing mMCP-2 as they present at the tips of the villi, the base of the villi, and the submucosa, respectively. That MC can reversibly alter their protease phenotypes suggests that a static nomenclature with fixed functional implications is inadequate to describe MC populations during an inflammatory process within a particular tissue.