The purpose of this paper is to review current infor-mation about the role of inflammation caused by He-licobacter pylori(H. pylori) infection in neurological diseases such as Parkinson's disease, Alzheimer's ...The purpose of this paper is to review current infor-mation about the role of inflammation caused by He-licobacter pylori(H. pylori) infection in neurological diseases such as Parkinson's disease, Alzheimer's dis-ease, 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 includ-ing chemokines [interleukin(IL)-8, macrophage che-motactic protein, growth-regulated oncogene(GRO)-α, chemokine(C-X-C motif) ligand 1] and cytokines [IL-1β, tumor necrosis factor-α, IL-6, IL-12, interferon-g], which can pass into the circulation and have a systemic effect. The persistence of detectable systemic and lo-cal 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 asso-ciated 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 combina-tion of multiple factors, but the systemic inflammatory response is a common component and determinant in the onset, evolution, and outcome of diseases. How-ever, more studies are needed to allow understanding of the effects and mechanisms by which the inflamma-tory response generated by H. pylori infection affects neurological diseases.展开更多
基金Supported by Hospital Infantil de México Federico Gómez,No.HIM/2012/018
文摘The purpose of this paper is to review current infor-mation about the role of inflammation caused by He-licobacter pylori(H. pylori) infection in neurological diseases such as Parkinson's disease, Alzheimer's dis-ease, 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 includ-ing chemokines [interleukin(IL)-8, macrophage che-motactic protein, growth-regulated oncogene(GRO)-α, chemokine(C-X-C motif) ligand 1] and cytokines [IL-1β, tumor necrosis factor-α, IL-6, IL-12, interferon-g], which can pass into the circulation and have a systemic effect. The persistence of detectable systemic and lo-cal 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 asso-ciated 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 combina-tion of multiple factors, but the systemic inflammatory response is a common component and determinant in the onset, evolution, and outcome of diseases. How-ever, more studies are needed to allow understanding of the effects and mechanisms by which the inflamma-tory response generated by H. pylori infection affects neurological diseases.
