Qi Ge, Hua Hong, Gao Yan, Lin Qin, Yu Guang-yan
Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology, Beijing 100081, China.
Chin Med J (Engl). 2007 Aug 20;120(16):1426-31.
Sjögren syndrome (SS) is an autoimmune disorder characterized by chronic lymphocytic infiltration and decreased secretion in salivary glands. Apoptosis is one of the possible mechanisms involved in acinar epithelial destruction in SS. The role of apoptosis in the initiation and effect phase of sialoadenitis is still controversial. The aim of this study was to observe the roles of apoptosis-associated proteins and serum IgG levels in sialoadenitis progression in nonobese diabetic (NOD) mice.
2-, 5-, 10-, 15-, 20-week female NOD and matched BALB/c control mice were selected. Saliva and tear flow rate were measured. Serum IgG level was tested by enzyme-linked immunosorbent assay (ELISA). Number of lymphocyte foci (NLF) in submandibular glands (SMGs) was counted under routine hematoxylin/eosin-stained sections. Expression of Fas, Bcl-2 and procaspase3 proteins as well as apoptotic cells in the SMGs were detected by immunohistochemical staining and by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay respectively.
Decreased stimulated total flow rate (STFR) and lymphocyte foci in SMGs were first observed in the 10-week NOD group. STFR was negatively correlated with NLF (P < 0.05). Serum IgG in NOD mice was significantly higher than that of the control group (P < 0.05) and showed a positive correlation with NLF (P < 0.05). Fas expression in SMGs acinar cells in NOD mice increased with age and was significantly higher compared with that in the control group. Bcl-2 expression and procaspase3 expression in SMG acinar cells in each NOD group were lower compared with those of the age-matched control mice.
Abnormal expression of Fas and Bcl-2 in the SMGs and higher level of serum IgG may contribute to the initiation of sialoadenitis and cause the glandular destruction in NOD mice.
干燥综合征（SS）是一种自身免疫性疾病，其特征为唾液腺慢性淋巴细胞浸润和分泌减少。细胞凋亡是干燥综合征腺泡上皮破坏可能涉及的机制之一。细胞凋亡在涎腺炎起始阶段和效应阶段的作用仍存在争议。本研究旨在观察细胞凋亡相关蛋白及血清IgG水平在非肥胖糖尿病（NOD）小鼠涎腺炎进展中的作用。
选取2周、5周、10周、15周、20周龄的雌性NOD小鼠及相匹配的BALB/c对照小鼠。测量唾液和泪液流速。采用酶联免疫吸附测定（ELISA）检测血清IgG水平。在苏木精/伊红常规染色切片下计数下颌下腺（SMG）中淋巴细胞灶数量（NLF）。分别通过免疫组织化学染色和末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）法检测SMG中Fas、Bcl-2和procaspase3蛋白的表达以及凋亡细胞。
10周龄NOD组首次观察到刺激后总流速（STFR）降低和SMG中淋巴细胞灶减少。STFR与NLF呈负相关（P < 0.05）。NOD小鼠血清IgG显著高于对照组（P < 0.05），且与NLF呈正相关（P < 0.05）。NOD小鼠SMG腺泡细胞中Fas表达随年龄增加，且显著高于对照组。各NOD组SMG腺泡细胞中Bcl-2表达和procaspase3表达均低于年龄匹配的对照小鼠。
SMG中Fas和Bcl-2的异常表达以及血清IgG水平升高可能导致NOD小鼠涎腺炎的起始并引起腺体破坏。
