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在干燥综合征的慢性炎症性病变中,血管新生明显。

Neovascularization is prominent in the chronic inflammatory lesions of Sjögren's syndrome.

出版信息

Int J Exp Pathol. 2014 Apr;95(2):131-7. doi: 10.1111/iep.12061.

Abstract

Angiogenesis is a common finding in chronic inflammatory diseases; however, its role in Sjögren's syndrome (SS) remains to be elucidated. Previous SS studies have demonstrated an increase in VEGF-A/VEGFR-2 system expression in minor salivary gland (MSG) biopsies from patients with SS, but differences in the new blood vessel formation between the different grades of disease severity have not been reported. Therefore, experiments were performed to demonstrate angiogenesis during different phases of primary SS (pSS) and to define the relationship between the microvessel density (MVD), macrophage infiltration and histiocyte distribution in SS MSG inflammatory lesions. In this series of experiments, immunohistochemistry was used to examine angiogenesis in serial sections of pSS MSG. Patients with pSS were classified accordingly with the grade of inflammatory lesions as I = low-grade (low focus score of 1 or 2), II = intermediate-grade (focus score of 3–6) and III = extensive inflammation in the MSG (high focus score of 12). Histological examination demonstrated that the MVD increased with the severity of the inflammatory lesions, and in addition, we found an increased infiltration of inflammatory and pro-angiogenic cells.These findings reveal that angiogenesis is intimately involved in the progression of pSS, may be central to the propagation of the chronic immune response observed in pSS and could represent a novel potential biomarker of pSS disease activity.

摘要

血管生成是慢性炎症性疾病的常见现象;然而,其在干燥综合征(SS)中的作用仍有待阐明。以前的 SS 研究表明,SS 患者的小唾液腺(MSG)活检中 VEGF-A/VEGFR-2 系统表达增加,但疾病严重程度不同的新血管形成之间的差异尚未报道。因此,进行了实验以证明原发性 SS(pSS)的不同阶段的血管生成,并定义 SS MSG 炎症病变中微血管密度(MVD)、巨噬细胞浸润和组织细胞分布之间的关系。在这一系列实验中,使用免疫组织化学检查 pSS MSG 的连续切片中的血管生成。根据 MSG 炎症病变的程度将 pSS 患者分类为 I = 低级别(低焦点评分 1 或 2)、II = 中级(焦点评分 3-6)和 III = MSG 中的广泛炎症(高焦点评分 12)。组织学检查表明 MVD 随着炎症病变的严重程度增加,此外,我们发现炎症和促血管生成细胞的浸润增加。这些发现表明血管生成与 pSS 的进展密切相关,可能是 pSS 中观察到的慢性免疫反应传播的核心,并且可能代表 pSS 疾病活动的新的潜在生物标志物。

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