title: Sialoadenitis progression in nonobese diabetic mice and its correlation with expression of apoptosis-associated proteins in salivary glands and serum IgG levels.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology, Beijing 100081, China.
authors.forename: Ge
authors.initials: G
authors.lastname: Qi
authors.forename: Hong
authors.initials: H
authors.lastname: Hua
authors.forename: Yan
authors.initials: Y
authors.lastname: Gao
authors.forename: Qin
authors.initials: Q
authors.lastname: Lin
authors.forename: Guang-yan
authors.initials: GY
authors.lastname: Yu
mesh_terms: D000818:Animals; D017209:Apoptosis; D053148:Caspase 3 / Q000032:analysis; D018450:Disease Progression; D005260:Female; D007074:Immunoglobulin G / Q000097:blood*; D051379:Mice; D008807:Mice, Inbred BALB C; D016688:Mice, Inbred NOD; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000032:analysis; D012469:Salivary Glands / Q000473:pathology; D012793:Sialadenitis / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D013363:Submandibular Gland / Q000737:chemistry; D019014:fas Receptor / Q000032:analysis