McArthur C P, Daniels P J, Kragel P, Howard P F, Julian L
Department of Oral Biology, School of Dentistry, University of Missouri-Kansas City 64108, USA.
J Autoimmun. 1997 Feb;10(1):59-65. doi: 10.1006/jaut.1996.0109.
Previous studies have demonstrated increased expression of a laminin-like protein in labial salivary glands from Sjögren's syndrome (SS) patients. The objective of the present study was to verify the identity of this protein and to compare lymphocytic infiltration and laminin expression in minor salivary gland ductal epithelium. This was carried out by comparing laminin protein and laminin mRNA expression in 13 SS patients, 11 normal controls, and 12 patients with non-specific sialoadenitis. Laminin protein and laminin mRNA expression was determined using immunoperoxidase (IP) and in situ hybridization (ISH) techniques, respectively. In addition, the relationship between lymphocytic infiltration and laminin expression was evaluated on adjacent serial salivary gland sections from SS patients, using routine histological methods and IP immunohistochemistry. Biopsies from SS patients showed significant increases in staining for both laminin protein and laminin mRNA compared to normal controls. On seven of the eight SS samples that showed significant laminin protein staining, the ductal epithelial staining occurred in the absence of periductal lymphocytic foci. Results of the ISH assay strongly suggest that the increased expression of the laminin-like protein is laminin, since the cDNA probe was specific for the B1 chain of laminin. In addition, this increased expression in ductal epithelial cells occurs without significant lymphocytic infiltration. These studies provide further evidence that altered laminin expression is an early event associated with salivary gland pathology in SS, since these data demonstrate a potential pathologic event prior to the arrival of lymphocytes. Further studies are underway to examine the relationship between laminin and lymphocytic infiltration in salivary gland pathology.
以往的研究表明,干燥综合征(SS)患者唇腺中一种层粘连蛋白样蛋白的表达增加。本研究的目的是验证该蛋白的身份,并比较小唾液腺导管上皮中的淋巴细胞浸润和层粘连蛋白表达。通过比较13例SS患者、11例正常对照者和12例非特异性涎腺炎患者的层粘连蛋白蛋白和层粘连蛋白mRNA表达来进行此项研究。分别使用免疫过氧化物酶(IP)和原位杂交(ISH)技术测定层粘连蛋白蛋白和层粘连蛋白mRNA表达。此外,使用常规组织学方法和IP免疫组织化学,在SS患者相邻的连续唾液腺切片上评估淋巴细胞浸润与层粘连蛋白表达之间的关系。与正常对照相比,SS患者的活检显示层粘连蛋白蛋白和层粘连蛋白mRNA的染色均显著增加。在显示显著层粘连蛋白蛋白染色的8个SS样本中的7个中,导管上皮染色发生在无导管周围淋巴细胞灶的情况下。ISH分析结果强烈表明,层粘连蛋白样蛋白表达增加的是层粘连蛋白,因为cDNA探针是层粘连蛋白B1链特异性的。此外,导管上皮细胞中的这种表达增加在无明显淋巴细胞浸润的情况下发生。这些研究提供了进一步的证据,表明层粘连蛋白表达改变是SS中与唾液腺病理相关联的早期事件,因为这些数据证明了在淋巴细胞到达之前的潜在病理事件。正在进行进一步研究以检查唾液腺病理中层粘连蛋白与淋巴细胞浸润之间的关系。