Published online Nov 15, 2014. doi: 10.4291/wjgp.v5.i4.400
Revised: March 30, 2014
Accepted: July 17, 2014
Published online: November 15, 2014
The purpose of this paper is to review current information about the role of inflammation caused by Helicobacter pylori (H. pylori) infection in neurological diseases such as Parkinson’s disease, Alzheimer’s disease, Guillain-Barré syndrome, multiple sclerosis, and other inflammatory diseases including ischemic stroke. Infection with H. pylori usually persists throughout life, resulting in a chronic inflammatory response with local secretion of numerous inflammatory mediators including chemokines [interleukin (IL)-8, macrophage chemotactic protein (MCP)-1, growth-regulated oncogene (GRO)-α] and cytokines [IL-1β, tumor necrosis factor (TNF)-α, IL-6, IL-12, interferon (IFN)-γ], which can pass into the circulation and have a systemic effect. The persistence of detectable systemic and local concentrations of inflammatory mediators is likely to alter the outcome of neurological diseases. These proinflammatory factors can induce brain inflammation and the death of neurons and could eventually be associated to Parkinson’s disease and also may be involved in the development of Alzheimer’s disease. However, most neurological diseases are the result of a combination of multiple factors, but the systemic inflammatory response is a common component and determinant in the onset, evolution, and outcome of diseases. However, more studies are needed to allow understanding of the effects and mechanisms by which the inflammatory response generated by H. pylori infection affects neurological diseases.
Core tip: Neurological diseases such as Parkinson, Alzheimer, Guillain-Barré syndrome, multiple sclerosis, and ischemic stroke are the result of a combination of multiple factors, but the chronic and systemic inflammatory response to Helicobacter pylori could be a common component and determinant in the onset, evolution, and outcome of these diseases.