Helicobacter pylori and neurological diseases: Married by the laws of inflammation

Abstract

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.

Keywords: Gastrointestinal diseases; Helicobacter pylori; Immune disease; Mediators of inflammation; Neurodegenerative diseases.

Figure 1

The inflammatory response in Helicobacter pylori infection. Immune cells are recruited to the lamina propria of the gastric epithelium by chemokines and cytokines (IL-8, MCP-1, GRO-α, IL-1β, TNF-α) produced by epithelial cells or directly by bacterial products including H. pylori neutrophil-activating protein, VacA, and urease. At the site of infection, the immune cells are activated and exert their effector functions, including the production of cytokines (IL-1β, TNF-α, IL-6, IL-12, IFN-γ, chemokines (IL-8, MCP-1), proteolytic enzymes, oxide nitric (NO) and reactive oxygen species (ROS). PG: Peptidoglycan; T4SS: Type IV secretion system; IL: Interleukin; TNF: Tumor necrosis factor; MCP: Macrophage chemotactic protein; GRO: Growth-regulated oncogene.