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The accumulation of inflammatory cells in synovial sheath and epitenon during adhesion formation in healing rat flexor tendons.

机译:在愈合大鼠屈肌腱的粘连过程中,滑膜鞘和上皮中炎性细胞的积累。

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摘要

The accumulation of inflammatory cells in synovial tissue was studied using indirect immunofluorescence assays on cell cultures and frozen tissue sections of healing rat digital flexor tendons. Flexor tendons were collected from rats 3, 7 and 14 days after crush injury. Tendon sheath and epithenon cells were isolated by sequential enzymic digestion and cultured for 2 days. Subpopulations of synovial and inflammatory cells were identified with MoAbs against cell surface glycoproteins present on B lymphocytes (CD45), T lymphocytes (CD2, CD4, CD8), macrophages (CD14) and endothelial cells. A phagocytosis assay was also used to identify macrophages. We report a substantial increase in the number of T lymphocytes (mainly helper/inducer) and phagocytotic cells with monocyte/macrophage surface markers in tendon sheath and epitenon 3 days after crush injury. The infiltration of inflammatory cells into synovial sheath and epitenon preceded an increase in fibronectin production by tendon cells which was seen 7 days after injury. To study the interaction between T lymphocytes and synovial cells in vitro, we established synovial fibroblast-like type B cell cultures and used stimulated and non-stimulated T lymphocytes in cell binding assays. We observed increased adhesiveness between unstimulated synovial cells and synovial cells previously cultured with activated and non-activated T lymphocytes. ELISA inhibition studies have shown an increase in fibronectin production by synovial fibroblasts co-cultured with stimulated CD4+ T lymphocytes. We suggest that the presence of inflammatory cells in synovial sheath and epitenon during tendon healing induces synovial fibroblasts and epitenon cells to increase their production of fibronectin, which provides a scaffold for subsequent adhesion formation.
机译:使用间接免疫荧光分析法对愈合的大鼠指屈肌腱的细胞培养物和冷冻组织切片进行研究,研究了滑膜组织中炎性细胞的积累。挤压伤后3、7和14天从大鼠收集屈肌腱。通过连续的酶消化分离肌腱鞘和上皮细胞,并培养2天。滑膜和炎性细胞的亚群被MoAbs鉴定为针对B淋巴细胞(CD45),T淋巴细胞(CD2,CD4,CD8),巨噬细胞(CD14)和内皮细胞上存在的细胞表面糖蛋白。吞噬作用测定法也用于鉴定巨噬细胞。我们报告挤压伤后3天,腱鞘和上皮中的T淋巴细胞(主要是辅助细胞/诱导细胞)和吞噬细胞以及单核细胞/巨噬细胞表面标志物的吞噬细胞数量显着增加。在损伤后7天观察到,在肌腱细胞产生纤连蛋白增加之前,炎性细胞渗透到滑膜鞘和表皮中。为了研究体外T淋巴细胞与滑膜细胞之间的相互作用,我们建立了滑膜成纤维细胞样B型细胞培养物,并在细胞结合试验中使用了受刺激的和未受刺激的T淋巴细胞。我们观察到未刺激的滑膜细胞和先前与活化和未活化的T淋巴细胞培养的滑膜细胞之间的粘附性增加。 ELISA抑制研究表明,与刺激的CD4 + T淋巴细胞共培养的滑膜成纤维细胞增加了纤连蛋白的产量。我们建议,在腱愈合过程中滑膜鞘和上皮中炎性细胞的存在诱导滑膜成纤维细胞和上皮细胞增加其纤连蛋白的产生,从而为随后的粘连形成提供支架。

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  • 作者

    Wojciak, B; Crossan, J F;

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  • 年度 2008
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  • 正文语种 en
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