Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Eicosenoids Modify Experimental Allergic Encephalomyelitis.

Anthony T. Reder1, Manjula Thapar, Anna Maria Sapugay

  • 1The University of Chicago Department of Neurology, and the Brain Research Institute Chicago, USA.

American Journal of Therapeutics
|September 1, 1995
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same journal

Abrocitinib as a Novel Therapeutic Option for Elastolytic Giant Cell Granuloma: A Case Report.

American journal of therapeutics·2026
Same journal

Dupilumab for Lichen Amyloidosis in an Elderly Multimorbid Patient.

American journal of therapeutics·2026
Same journal

Deucravacitinib for Generalized Pustular Psoriasis and Comorbid Polymyositis: Dual Efficacy and Favorable Safety.

American journal of therapeutics·2026
Same journal

Repurposed Drugs and Cardiovascular Morbidity: A Cost-Effectiveness Analysis.

American journal of therapeutics·2026
Same journal

Do Not Treat a Sequencing Report: Therapeutic Stewardship in Endometrial Microbiome Testing.

American journal of therapeutics·2026
Same journal

Right Side Accessory Pathway Mediated Cardiomyopathy Treated with Amiodarone: First Adult Case Report.

American journal of therapeutics·2026

Prostaglandin E (PGE) analogs and leukotriene (LKT) synthesis inhibitors show promise in treating autoimmune brain diseases like multiple sclerosis (MS). These compounds modulate immune responses by altering cyclic AMP and cyclic GMP levels, reducing central nervous system inflammation.

Area of Science:

  • Neuroimmunology
  • Autoimmune Diseases
  • Pharmacology

Background:

  • Experimental allergic encephalomyelitis (EAE) is a key animal model for multiple sclerosis (MS) and postinfectious encephalomyelitis.
  • In EAE and MS, immune cells like monocytes and Th1 lymphocytes breach the blood-brain barrier, leading to demyelination and neuronal damage.
  • Prostaglandin E (PGE), a product of monocytes and glial cells, plays a role in immune regulation, with cAMP agonists inhibiting Th1 cell activity.

Purpose of the Study:

  • To investigate the potential of eicosanoids, specifically PGE analogs and leukotriene (LKT) synthesis inhibitors, in mitigating central nervous system inflammation in EAE.
  • To explore the combined effects of PGE analogs and LKT synthesis inhibitors on EAE and related immune responses.

Main Methods:

  • Administration of misoprostol (a PGE1 analog) and indomethacin (an inhibitor of PGE synthesis) in Lewis rats with EAE.

Related Experiment Videos

  • Evaluation of clinical and histological signs of EAE, delayed-type hypersensitivity reactions, and in vitro lymphocyte proliferation.
  • Assessment of leukotriene (LKT) synthesis inhibitors' effects on EAE and their synergy with PGE analogs.

    • Main Results:

    • Misoprostol and indomethacin significantly inhibited clinical and histological manifestations of EAE, whether administered early or at disease onset.
    • The combination of misoprostol and indomethacin suppressed Th1 responses, including delayed-type hypersensitivity to myelin basic protein (MBP) and in vitro lymphocyte proliferation.
    • Inhibitors of LKT synthesis blocked EAE, suggesting a role for cGMP in inflammatory cell function, and enhanced the therapeutic effects of misoprostol and indomethacin.

    Conclusions:

    • PGE analogs, indomethacin, and LKT synthesis inhibitors effectively suppress autoimmune responses against brain antigens in vitro and in vivo.
    • Modulating intracellular cAMP and cGMP levels using these agents presents a potential therapeutic strategy for inflammatory and autoimmune neurological diseases.
    • Targeting eicosanoid pathways offers a promising avenue for developing treatments for conditions like multiple sclerosis.