title: A longitudinal study on an autoimmune murine model of ankylosing spondylitis.
abstract: BACKGROUND
  Proteoglycan aggrecan (PG)-induced arthritis (PGIA) is the only systemic autoimmune murine model which affects the axial skeleton, but no studies have been performed characterising the progression of spine involvement.
  
  
  OBJECTIVE
  To follow pathological events in experimental spondylitis, and underline its clinical, radiographic, and histological similarities to human ankylosing spondylitis (AS); and to determine whether the spondyloarthropathy is a shared phenomenon with PGIA, or an "independent" disease.
  
  
  METHODS
  Arthritis/spondylitis susceptible BALB/c and resistant DBA/2 mice, and their F1 and F2 hybrids were immunised with cartilage PG, and radiographic and histological studies were performed before onset and weekly during the progression of spondylitis.
  
  
  RESULTS
  About 70% of the PG immunised BALB/c mice develop spondyloarthropathy (proteoglycan-induced spondylitis (PGISp), and the progression of the disease is very similar to human AS. It begins with inflammation in the sacroiliac joints and with enthesitis, and then progresses upwards, affecting multiple intervertebral disks. In F2 hybrids of arthritis/spondylitis susceptible BALB/c and resistant DBA/2 mice the incidence of arthritis was 43.5%, whereas the incidence of spondylitis was >60%. Some arthritic F2 hybrid mice had no spondylitis, whereas others developed spondylitis in the absence of peripheral arthritis.
  
  
  CONCLUSIONS
  The PGISp model provides a valuable tool for studying autoimmune reactions in spondylitis, and identifying genetic loci associated with spondyloarthropathy.
authors.affiliation: Department of Orthopedic Surgery, Rush University Medical Center, Cohn Research Building, Room 708, 1735 W Harrison Street, Chicago, IL 60612, USA.
authors.forename: T
authors.initials: T
authors.lastname: Bárdos
authors.forename: Z
authors.initials: Z
authors.lastname: Szabó
authors.forename: M
authors.initials: M
authors.lastname: Czipri
authors.forename: C
authors.initials: C
authors.lastname: Vermes
authors.forename: M
authors.initials: M
authors.lastname: Tunyogi-Csapó
authors.forename: R M
authors.initials: RM
authors.lastname: Urban
authors.forename: K
authors.initials: K
authors.lastname: Mikecz
authors.forename: T T
authors.initials: TT
authors.lastname: Glant
mesh_terms: D000818:Animals; D001169:Arthritis, Experimental / Q000276:immunology / Q000473:pathology; D001327:Autoimmune Diseases / Q000276:immunology / Q000473:pathology; D004195:Disease Models, Animal; D018450:Disease Progression; D005260:Female; D007114:Immunization; D007403:Intervertebral Disc / Q000276:immunology / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D008811:Mice, Inbred DBA; D023421:Models, Animal; D011509:Proteoglycans; D012446:Sacroiliac Joint / Q000276:immunology / Q000473:pathology; D013167:Spondylitis, Ankylosing / Q000139:chemically induced / Q000276:immunology* / Q000473:pathology
chemical_list: D011509:Proteoglycans