Does gamma-aminobutyric acid (GABA) influence the development of chronic inflammation in rheumatoid arthritis?
- PDF / 574,277 Bytes
- 5 Pages / 610 x 792 pts Page_size
- 31 Downloads / 193 Views
BioMed Central
Open Access
Hypothesis
Does gamma-aminobutyric acid (GABA) influence the development of chronic inflammation in rheumatoid arthritis? James M Kelley, Laura B Hughes and S Louis Bridges Jr* Address: Division of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA Email: James M Kelley - [email protected]; Laura B Hughes - [email protected]; S Louis Bridges* - [email protected] * Corresponding author
Published: 3 January 2008 Journal of Neuroinflammation 2008, 5:1
doi:10.1186/1742-2094-5-1
Received: 28 October 2007 Accepted: 3 January 2008
This article is available from: http://www.jneuroinflammation.com/content/5/1/1 © 2008 Kelley et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract Background: Recent studies have demonstrated a role for spinal p38 MAP kinase (MAPK) in the development of chronic inflammation and peripheral arthritis and a role for GABA in the inhibition of p38 MAPK mediated effects. Integrating these data suggests that GABA may play a role in downregulating mechanisms that lead to the production of proinflammatory agents such as interleukin-1, interleukin-6, and matrix metalloproteinase 3 – agents implicated in the pathogenesis of rheumatoid arthritis (RA). Genetic studies have also associated RA with members of the p38 MAPK pathway. Hypothesis: We propose a hypothesis for an inefficient GABA signaling system that results in unchecked proinflammatory cytokine production via the p38 MAPK pathway. This model also supports the need for increasing research in the integration of immunology and neuroscience.
Background The impact of an immune response on the nervous system has long been apparent, with multiple sclerosis (MS), myasthenia gravis (MG), and neuropsychiatric manifestations of systemic lupus erythematosus serving as examples. While neuroendocrine modulation of the immune system has been appreciated, the influence of the nervous system on immune responses is not well understood. The complex characters of a coordinated immune response and the nervous/endocrine (electrical/ chemical) communication systems of the body complicate research in this area; however, relationships between the nervous and immune systems are essential for proper function. Any entity would be compromised if its defense and communication systems did not interact – humans are no exception.
Rheumatoid arthritis (RA) is a common systemic inflammatory condition leading to symmetric, chronic synovial inflammation, erosions, and joint destruction in some patients. Its etiology is unclear but may result from an environmental trigger in the context of genetic predisposition. There is literature precedent for neuroendocrine involvement in RA pathogenesis [1] including suggestions of n
Data Loading...
