Related Experiment Video
Updated: Jun 1, 2026
Flow Cytometric Analysis of Lymphocyte Infiltration in Central Nervous System during Experimental Autoimmune Encephalomyelitis
Published on: November 17, 2020
Cyclooxygenase expression and prostaglandin levels in central nervous system tissues during the course of chronic
Samir S Ayoub1, Elizabeth G Wood, Sabih-Ul Hassan
1Centre for Biochemical Pharmacology, William Harvey Research Institute, St. Bartholomew's and London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.
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 PGE(2) and PGD(2), 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. PGE(2) and PGD(2) 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. PGE(2) and PGD(2) 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 PGE(2) and PGD(2) 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.
Insights
Cyclooxygenase (COX) enzyme expression and prostaglandin (PG) levels were studied in chronic relapsing experimental autoimmune encephalomyelitis (CR EAE). Elevated COX-1, COX-1b, and PG levels during relapse suggest therapeutic targets for CNS inflammation.
Area of Science:
- Neuroimmunology
- Inflammation research
- Prostaglandin biology
Background:
- Multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) are characterized by significant central nervous system (CNS) inflammation.
- Prostaglandins (PGs) are key mediators implicated in the pathology of MS and EAE.
- Cyclooxygenase (COX) enzymes generate prostaglandins.
Purpose of the Study:
- To investigate the expression of COX isoenzymes (COX-1, COX-1b, COX-2) and the levels of PGE(2) and PGD(2) in CNS tissues during the development of chronic relapsing EAE (CR EAE).
- To explore the relationship between COX isoenzyme expression and PG levels during different neurological phases of CR EAE.
Main Methods:
- CR EAE was induced in Biozzi mice.
- Cerebral cortex, cerebellum, and spinal cord tissues were collected during acute, remission, and relapse stages.
- COX enzyme expression was analyzed using Western blotting.
- PGE(2) and PGD(2) levels were quantified via enzyme immunoassay kits.
Main Results:
- COX-2 expression in spinal cords was unaltered during acute disease.
- COX-1, COX-1b, and COX-2 expression increased in other sampled CNS areas during acute disease.
- PGE(2) and PGD(2) levels remained unchanged during acute and remission phases.
- COX-1 and COX-1b expression, along with PGE(2) and PGD(2) concentrations, were markedly elevated during the relapse stage of CR EAE.
Conclusions:
- COX isoenzyme expression patterns and PG levels change dynamically throughout the course of CR EAE.
- Elevated COX-1 and COX-1b expression, along with increased PGE(2) and PGD(2) during relapse, highlight their role in CNS inflammation.
- Therapeutic strategies targeting PG-mediated inflammation should be considered for administration before or during the relapse phase of CR EAE.
