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Updated: Aug 25, 2026
Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
Published on: May 8, 2016
Protective effects of histamine H4 receptor antagonist on the inflammatory responses in B cells in a mouse model of
Haneen A Al-Mazroua1, Hussain N Alhamami1, Ahmed Nadeem1
1Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, Kingdom of Saudi Arabia.
Background:
Multiple sclerosis (MS) is an inflammatory, demyelinating, and neurodegenerative disease of the central nervous system (CNS) driven by autoimmune mechanisms. However, growing evidence indicates that B lymphocytes may contribute to the disease through antigen presentation and the production of proinflammatory mediators. This study aimed to examine the effect of JNJ 10191584 (JNJ), a potent and selective H4R antagonist, on EAE progression and to uncover the underlying mechanisms.
Methods:
The research explored the potential impact of H4R antagonists on inflammatory responses in B cells within an EAE mouse model of MS. EAE mice received an oral dose of JNJ at 6 mg/kg daily, starting on day 10 and continuing until day 42. Flow cytometry assessed JNJ's effect on the expression of NF-κB p65, IκBα, Notch1, Notch3, IL-2, IL-6, GM-CSF, iNOS, TNF-α, and MCP-1 in CD19+ B cells. We used RT-PCR to assess the impact of JNJ on mRNA levels of these inflammatory markers in brain tissue.
Results:
In EAE mice, JNJ treatment reduced the number of CD19+ cells expressing NF-κB p65, IκBα, Notch1, Notch3, IL-2, IL-6, GM-CSF, iNOS, and MCP-1. Additionally, JNJ decreased mRNA expression of inflammatory markers in brain tissue compared with vehicle-treated mice.
Conclusions:
These results suggest that targeting H4R with antagonists could offer a new therapeutic approach for MS by specifically modulating B-cell-mediated inflammation.
