title: Upregulation of antibody response to heat shock proteins and tissue antigens in an ocular ischemia model.
abstract: OBJECTIVE
  The aim of this study was to characterize the serum antibody reactivities occurring after ocular ischemia reperfusion. The time course of serum antibody responses was examined.
  
  
  METHODS
  Wistar rats were exposed to transient ocular ischemia by elevating intraocular pressure to 130 mm Hg for 60 minutes. Axonal damage was evaluated on optic-nerve sections 2 and 4 weeks later. Blood samples collected before and several times after ischemia were used for antibody detection via customized protein microarrays. Different tissue antigens, including heat shock proteins (HSPs) and crystallins, were selected based on previous identification of antibody reactivities in studies on ischemic events or ophthalmic diseases associated with ischemia. Antibody reactivity was compared using multivariate statistical techniques.
  
  
  RESULTS
  Significant axonal damage was observed 2 and 4 weeks after ocular ischemia (P < 0.05). Animals showed certain immunoreactivities against antigens even before ischemia, whereas many reactivities increased afterward. Significantly different responses were detected 2, 3, and 4 weeks after ischemia (P < 0.05). Antibody reactivity against actin, glial fibrillary acidic protein, HSP 27, vimentin, or spectrin continually increased.
  
  
  CONCLUSIONS
  Ischemia induced by acute intraocular pressure elevation led to complex changes in antibody reactivities in sera of treated animals. Upregulation of serum autoantibodies, especially against heat shock and structural proteins, progressively increased throughout the 4-week follow-up period, whereas others such as ubiquitin decreased. The upregulation of anti-HSP 27 antibodies might be an attempt to protect the tissue from ischemic damage.
authors.affiliation: Center for Vision Science, Ruhr University Eye Hospital, Bochum, Germany.
authors.forename: Stephanie C
authors.initials: SC
authors.lastname: Joachim
authors.forename: Martin B
authors.initials: MB
authors.lastname: Wax
authors.forename: Nils
authors.initials: N
authors.lastname: Boehm
authors.forename: Desiree R
authors.initials: DR
authors.lastname: Dirk
authors.forename: Norbert
authors.initials: N
authors.lastname: Pfeiffer
authors.forename: Franz H
authors.initials: FH
authors.lastname: Grus
mesh_terms: D000818:Animals; D001323:Autoantibodies / Q000097:blood*; D001324:Autoantigens / Q000276:immunology*; D001369:Axons / Q000473:pathology; D005136:Eye Proteins / Q000276:immunology*; D005904:Glial Fibrillary Acidic Protein / Q000276:immunology; D055551:HSP27 Heat-Shock Proteins / Q000276:immunology*; D007074:Immunoglobulin G / Q000097:blood; D007429:Intraocular Pressure; D008297:Male; D004676:Myelin Basic Protein / Q000276:immunology; D009185:Myelin Proteins; D018992:Myelin-Associated Glycoprotein / Q000276:immunology; D063308:Myelin-Oligodendrocyte Glycoprotein; D009900:Optic Nerve / Q000473:pathology; D040081:Protein Array Analysis; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000276:immunology*; D012164:Retinal Diseases / Q000276:immunology*; D012171:Retinal Vessels; D013049:Spectrin / Q000276:immunology; D015854:Up-Regulation
chemical_list: D001323:Autoantibodies; D001324:Autoantigens; D005136:Eye Proteins; D005904:Glial Fibrillary Acidic Protein; D055551:HSP27 Heat-Shock Proteins; C486114:Hspb1 protein, rat; D007074:Immunoglobulin G; C571328:Mog protein, rat; D004676:Myelin Basic Protein; D009185:Myelin Proteins; D018992:Myelin-Associated Glycoprotein; D063308:Myelin-Oligodendrocyte Glycoprotein; D013049:Spectrin