Is damage in central nervous system due to inflammation?
The aim of this work was to review the inflammatory factors involved in central nervous system (CNS) inflammation and the damage associated to their participation in an inflammatory disease of CNS, multiple sclerosis in humans and experimental allergic encephalomyelitis in the murine model. Inflammation has an important repairing function, nevertheless frequently in the CNS inflammation is the cause of damage and it does not fulfill this repairing function as it happens in other compartments of the body. The inflammatory response in the CNS involves the participation of different cellular types of the immune system (macrophages, mast cells, T and B lymphocytes, dendritic cells) and resident cells of the CNS (microglia, astrocytes, neurons), adhesion molecules, cytokines and chemokines among other proteic components. During neuroinflammation chemotaxis is an important event in the recruitment of cells to the CNS. The lymphocyte recruitment implies the presence of chemokines and chemokine receptors, the expression of adhesion molecules, the interaction between lymphocytes and the bloodbrain barrier (BBB) endothelium, and finally their passage through the BBB to arrive at the site of inflammation. If this process is not controlled, is prolonged, inflammation loses its repairing function and can be the cause of damage. Usually neuroinflammation has the tendency to decline to damage, which would explain most of the CNS pathologies.
Chavarria
A
A
Departamento de Inmunología, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, UNAM, AP70228, Mexico DF 04510, Mexico.
Alcocer-Varela
J
J
D000818:Animals; D000938:Antigen-Presenting Cells / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D002490:Central Nervous System / Q000276:immunology* / Q000473:pathology*; D018925:Chemokines / Q000378:metabolism; D002633:Chemotaxis; D016207:Cytokines / Q000378:metabolism; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology / Q000473:pathology; D006801:Humans; D007249:Inflammation; D007371:Interferon-gamma / Q000276:immunology; D008954:Models, Biological; D009103:Multiple Sclerosis / Q000276:immunology / Q000473:pathology; D013601:T-Lymphocytes / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
D018925:Chemokines; D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma