caa a22 4500 445885556 CHVBK 20180317145558.0 cr unu---uuuuu 170323e20111001xx s 000 0 eng 10.1007/s00011-011-0352-3 doi (NATIONALLICENCE)springer-10.1007/s00011-011-0352-3 Cyclooxygenase expression and prostaglandin levels in central nervous system tissues during the course of chronic relapsing experimental autoimmune encephalomyelitis (EAE) [Elektronische Daten] [Samir Ayoub, Elizabeth Wood, Sabih-Ul Hassan, Christopher Bolton] Objective: Multiple sclerosis (MS) and its animal counterpart experimental autoimmune encephalomyelitis (EAE) have a major inflammatory component that drives and orchestrates both diseases. One particular group of mediators are the prostaglandins (PGs), which we have previously shown, through quantitation and pharmacological intervention, to be closely involved in the pathology of MS and EAE. The aim of the current study was to determine the expression of the PG-generating cyclooxygenase (COX) enzymes and the profile of PGE2 and PGD2, in selected central nervous system (CNS) tissues, with the development of the chronic relapsing (CR) form of EAE. In particular, the work investigates the possible relationship between the expression of COX isoenzymes and PG levels during the neurological phases of CR EAE. Methods: CR EAE was induced in Biozzi mice with inoculum containing lyophilised, syngeneic spinal cord emulsified in complete Freund's adjuvant. The cerebral cortex, cerebellum and spinal cord were dissected from mice during the acute, remission and relapse stages of disease with a minimum of five animals per treatment. The expression of COX-1, COX-1b variant and COX-2, in pooled samples, was determined by Western blotting. PGE2 and PGD2 levels in extracted samples were measured using commercial enzyme immunoassay kits. Results: COX-2 expression in spinal cords during acute disease remained unaltered and was in contrast to an enhancement of the enzyme, together with COX-1 and COX-1b, in all other sampled areas. PGE2 and PGD2 levels remained unchanged during the acute phase and the subsequent remission of symptoms. COX-1 and COX-1b expression was elevated in tissues during the relapse stage of CR EAE and concentrations of the prostanoids were markedly increased. Conclusions: The study examines the implications of COX isoenzyme expression over the course of CR EAE and discusses the reported relationship between PGE2 and PGD2 in the instigation and resolution of CNS inflammation. Consideration is also given to the treatment of CR EAE and suggests that drugs designed to limit the inflammatory effects of the PGs should be administered prior to or during the relapse phase of the disease. Springer Basel AG, 2011 Cerebral cortex nationallicence Cyclooxygenase nationallicence Experimental autoimmune encephalomyelitis nationallicence Multiple sclerosis nationallicence Prostaglandin nationallicence Spinal cord nationallicence Ayoub Samir Centre for Biochemical Pharmacology, William Harvey Research Institute, St. Bartholomew's and the London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, EC1M 6BQ, London, UK aut Wood Elizabeth Centre for Translational Medicine and Therapeutics, Second Floor, John Vane Science Centre, Charterhouse Square, EC1M 6BQ, London, UK aut Hassan Sabih-Ul Centre for Biochemical Pharmacology, William Harvey Research Institute, St. Bartholomew's and the London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, EC1M 6BQ, London, UK aut Bolton Christopher Neuroimmunology Unit, Centre for Neuroscience and Trauma, Blizard Institute of Cell and Molecular Science, Barts and The London School of Medicine and Dentistry, 4, Newark Street, E12 AT, London, UK aut Inflammation Research SP Birkhäuser Verlag Basel 60/10(2011-10-01), 919-928 1023-3830 60:10<919 2011 60 11 https://doi.org/10.1007/s00011-011-0352-3 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00011-011-0352-3 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Ayoub Samir Centre for Biochemical Pharmacology, William Harvey Research Institute, St. Bartholomew's and the London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, EC1M 6BQ, London, UK aut NATIONALLICENCE 700 1- Wood Elizabeth Centre for Translational Medicine and Therapeutics, Second Floor, John Vane Science Centre, Charterhouse Square, EC1M 6BQ, London, UK aut NATIONALLICENCE 700 1- Hassan Sabih-Ul Centre for Biochemical Pharmacology, William Harvey Research Institute, St. Bartholomew's and the London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, EC1M 6BQ, London, UK aut NATIONALLICENCE 700 1- Bolton Christopher Neuroimmunology Unit, Centre for Neuroscience and Trauma, Blizard Institute of Cell and Molecular Science, Barts and The London School of Medicine and Dentistry, 4, Newark Street, E12 AT, London, UK aut NATIONALLICENCE 773 0- Inflammation Research SP Birkhäuser Verlag Basel 60/10(2011-10-01), 919-928 1023-3830 60:10<919 2011 60 11 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer