A Key Regulatory Role for Histamine in Experimental Autoimmune Encephalomyelitis: Disease Exacerbation in Histidine Decarboxylase-deficient Mice.
From: Immunology and Muscular Pathology Unit, National Neurological Institute “C. Besta,” Milan, Italy.
Journal of immunology (Baltimore, Md. : 1950)
- Publish Date: Jan 2006
- ISSN: 0022-1767
- Volume: 176
- Issue: 1
- Pages: 17-26
- Medium: Print
- Language: English
- Citation (JAMA): Musio Silvia, Gallo Barbara, Scabeni Stefano, et al. A Key Regulatory Role for Histamine in Experimental Autoimmune Encephalomyelitis: Disease Exacerbation in Histidine Decarboxylase-deficient Mice.. J. Immunol. Jan 2006;176:17-26
Abstract
Histamine can modulate the cytokine network and influence Th1 and Th2 balance and Ab-isotype switching. Thus, pharmacological blockade or genetic deletion of specific histamine receptors has been shown to reduce the severity of experimental autoimmune encephalomyelitis (EAE), a prototypic Th1-mediated disease with similarities to human multiple sclerosis. To study the comprehensive contribution of endogenous histamine to the expression of EAE, we attempted to induce EAE in histidine decarboxylase-deficient mice, which are genetically unable to make histamine. In this study, we show that EAE is significantly more severe in HDC-/-, histamine-deficient mice, with diffuse inflammatory infiltrates, including a prevalent granulocytic component, in the brain and cerebellum. Unlike splenocytes from wild-type mice, splenocytes from HDC-/- mice do not produce histamine in response to the myelin Ag, whereas production of IFN-gamma, TNF, and leptin are increased in HDC-/- splenocytes in comparison to those from wild-type mice. Endogenous histamine thus appears to regulate importantly the autoimmune response against myelin and the expression of EAE, in this model, and to limit immune damage to the CNS. Understanding which receptor(s) for histamine is/are involved in regulating autoimmunity against the CNS might help in the development of new strategies of treatment for EAE and multiple sclerosis.
Mesh Headings (Keywords): Animals, Brain, Chemokine CCL2, Encephalomyelitis, Autoimmune, Experimental, Glycoproteins, Histamine, Histidine Decarboxylase, Interferon Type II, Leptin, Mice, Peptide Fragments, T-Lymphocytes, Tumor Necrosis Factor-alpha
Check for Full Text / PubMed Unique Identifier (PMID): 16365391
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.