Role of nonspecific infection in the development of acute and chronic inflammatory diseases of the nervous system

Abstract

The paper presents an update on the susceptibility of the central nervous system (CNS) to inflammation in response to injury, infection, or disease. CNS resident cells generate inflammatory mediators, including proinflammatory cytokines, prostaglandins, free radicals, and a complement, which induce chemokines and adhesion molecules, recruit immune cells, and activate glial cells. Inflammation and inflammatory mediators, in turn, cause neurodegeneration and are thus involved in the pathogenesis of acute and chronic mental and CNS diseases. Information is given on the expression of inflammatory mediators, on the mechanisms that regulate inflammation, and on the CNS in brain injury, epilepsy, multiple sclerosis, Alzheimer's disease and Parkinson's disease. The integrative action of inflammatory mediators in combination with processes of ageing burdened with heredity and poor environmental factors plays an important role in the development and prolongation of chronic neurodegeneration and should be kept in mind during therapy for CNS diseases. Emphasis is placed on effective approaches to treating acute neurological impairments (stroke, injury) when the early use of an IL-1 receptor antagonist is of importance and on chronic inflammatory neurodegenerative processes when long-term anti-inflammatory therapy reducing the rate of relapses of the disease and its progression is indicated.

Keywords

central nervous system / inflammation / pathogenesis / acute and chronic inflammatory response / infection

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