title: BXSB/MpJ-Yaa mice develop autoimmune dacryoadenitis with the appearance of inflammatory cell marker messenger RNAs in the lacrimal fluid.
abstract: BACKGROUND
  Dacryoadenitis is characteristic of an autoimmune exocrinopathy, e.g. Sjögren syndrome. We pathologically examined the lacrimal glands of autoimmune-prone BXSB/MpJ-Yaa mice for the appearance of pathological signs of dacryoadenitis progression in autoimmune dacryoadenitis models, particularly focusing on messenger RNAs in the lacrimal fluid.
  
  
  METHODS
  The lacrimal glands of the BXSB/MpJ-Yaa and C57BL/6 mice were histopathologically analyzed in parallel with the evaluation of lacrimation and messenger RNA expression of water channels (Aqp3, Aqp4 and Aqp5). In addition, autoimmune model mice (MRL/MpJ-lpr/lpr and NZB/NZWF1) were used for evaluating cell infiltration and detecting inflammatory cell marker messenger RNAs (Cd68, Ptprc and Cd3e) in the lacrimal fluids by polymerase chain reaction-based methods.
  
  
  RESULTS
  B-cell predominant lymphocytic infiltrations and the destruction of acini were observed in the lacrimal glands of BXSB/MpJ-Yaa mice. There was no significant difference in the quantity of lacrimal fluid between the BXSB/MpJ-Yaa and C57BL/6 mice. In the BXSB/MpJ-Yaa mice, Aqp3 expression increased significantly with the cell infiltration score, whereas expression of Aqp4 and Aqp5 tended to decrease. Aqp3 expression increased significantly with the cell infiltration score in BXSB/MpJ-Yaa mice. Among inflammatory cell markers, Cd68 was more frequently detected in the lacrimal fluid of the BXSB/MpJ-Yaa, MRL/MpJ-lpr/lpr and NZB/NZWF1 mice than in that of the C57BL/6 mice.
  
  
  CONCLUSIONS
  BXSB/MpJ-Yaa mice clearly developed autoimmune dacryoadenitis. The altered expression of water channels in lacrimal glands might be associated with the preservation of lacrimal fluid excretion in BXSB/MpJ-Yaa mice. The detection of inflammatory cell markers in lacrimal fluid could be used as a diagnostic marker for autoimmune dacryoadenitis.
authors: Laboratory of Anatomy, Department of Biomedical Sciences, Hokkaido University, Sapporo, Japan.
authors: Keigo
authors: K
authors: Kosenda
authors: Osamu
authors: O
authors: Ichii
authors: Saori
authors: S
authors: Otsuka
authors: Yoshiharu
authors: Y
authors: Hashimoto
authors: Yasuhiro
authors: Y
authors: Kon
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000235:genetics; D015214:Antigens, Differentiation, Myelomonocytic / Q000235:genetics; D020346:Aquaporins / Q000235:genetics; D001327:Autoimmune Diseases / Q000175:diagnosis / Q000235:genetics / Q000276:immunology*; D001402:B-Lymphocytes / Q000502:physiology; D017252:CD3 Complex / Q000235:genetics; D003607:Dacryocystitis / Q000175:diagnosis / Q000235:genetics / Q000276:immunology*; D004195:Disease Models, Animal; D018450:Disease Progression; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D005819:Genetic Markers / Q000235:genetics*; D007765:Lacrimal Apparatus / Q000276:immunology / Q000473:pathology*; D017493:Leukocyte Common Antigens / Q000235:genetics; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D019463:Mice, Inbred MRL lpr; D008814:Mice, Inbred NZB; D008817:Mice, Mutant Strains; D012333:RNA, Messenger / Q000378:metabolism*; D060888:Real-Time Polymerase Chain Reaction; D013601:T-Lymphocytes / Q000502:physiology; D013666:Tears / Q000378:metabolism*; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D020346:Aquaporins; D017252:CD3 Complex; D005819:Genetic Markers; D017493:Leukocyte Common Antigens; D012333:RNA, Messenger; C081026:CD68 protein, mouse; D000097382:CD68 Molecule; C485468:Cd3e protein, mouse; C516770:Ptprc protein, mouse
keywords: BXSB/MpJ-Yaa; Sjögren syndrome; autoimmune dacryoadenitis; lacrimal fluid