Cellular and molecular alterations in spinal cord injury patients with pressure ulcers: a preliminary report.
Cellular and molecular alterations in spinal cord injury patients with pressure ulcers: a preliminary report.
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患有压疮的脊髓损伤患者的细胞和分子变化：初步报告。
DOI：
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发表时间：
2002
期刊：
影响因子：
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通讯作者：
S. Dilioglou
中科院分区：
文献类型：
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作者：
J. Cruse;Huan Wang;Robert E. Lewis;J. Cespedes;R. S. Morrison;W. Lineaweaver;S. Dilioglou
该研究旨在调查对脊髓损伤（SCI）患者伤口愈合至关重要的分子在数量和功能上的变化。压疮愈合延迟的脊髓损伤患者被用作研究对象。年龄匹配的健康个体作为对照。通过流式细胞术分析测量外周血白细胞（包括淋巴细胞和粒细胞）的粘附分子表达。使用人脐带静脉内皮细胞（HUVEC）作为结合基质评估淋巴细胞的结合能力。对患者压疮样本进行免疫染色，以确定纤连蛋白、加里宁、β4 整合素、α2β1、α3β1、α5β1 和 CD138 的表达。与健康对照相比，患者淋巴细胞群中 CD11a、CD11b、CD18、CD49b、CD49c、CD49d、CD54 和 CD8 的表达降低，粒细胞群中 CD11a、CD18、CD49c、CD49d 和 CD8 的表达降低。患者体内的结合能力（以淋巴细胞与 HUVEC 基质的结合百分比表示）大大降低。压疮中纤连蛋白的免疫组织化学染色明显减少。这些发现表明，SCI 患者压疮愈合延迟可归因于粘附分子表达减少、细胞间相互作用受损以及细胞外基质结构和功能蛋白的缺乏。
The study was designed to investigate the changes, both numerically and functionally, of the molecules critical to wound healing in spinal cord injury (SCI) patients. Spinal cord injury patients who demonstrated delayed healing of their pressure ulcers were used as study subjects. Age-matched healthy individuals served as controls. Adhesion molecule expression of the peripheral blood leukocytes, including lymphocytes and granulocytes, was measured by flow cytometric analysis. Binding capacity of the lymphocytes was evaluated using human umbilical cord vein endothelial cells (HUVECs) as the binding matrix. Samples from pressure ulcers of the patients were immunostained to define fibronectin, kalinin, beta4 integrin, alpha2beta1, alpha3beta1, alpha5beta1, and CD138 expression. Compared to healthy controls, there was decreased expression of CD11a, CD11b, CD18, CD49b, CD49c, CD49d, CD54, and CD8 in patients' lymphocyte populations and CD11a, CD18, CD49c, CD49d, and CD8 in patients' granulocyte populations. The binding capacity, expressed as percentage binding of the lymphocytes to the HUVEC matrix, was greatly diminished in the patients. There was markedly diminished immunohistochemical staining of fibronectin in pressure ulcers. These findings showed that delayed healing of pressure ulcers in SCI patients can be attributed to reduced adhesion molecule expression, impaired cell-cell interaction, and lack of extracellular matrix structural and functional protein.