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Additional info for Age-Related Macular Degeneration, 2nd Edition
Recently, the idea has emerged that certain kinds of chronic infections might cause (or at least contribute to) degenerative diseases that are not considered to be truly inﬂammatory (88–91). One of the most dramatic examples is peptic ulcer disease, recently recognized to be caused by infection of the gastric subepithelial mucosa with a gram-positive bacterium called Helicobacter pylori (92). Accordingly, ulcer disease is now treated by antibiotics and not with diet or surgery. Recently, chronic bacterial or viral infection of vascular endothelial cells has been suggested as an etiology for coronary artery atherosclerosis, and infection with an unusual agent called a prion has been shown as a cause of certain neurodegenerative diseases.
Innate Immunity in Glomerular Diseases Chronic Injury As is the case for atherosclerosis, a response to injury hypothesis has been substantiated for glomerulosclerosis due to aging, hypertension or diabetes (138–145). Glomerulosclerosis is characterized by progressive thickening of the glomerular extracellular matrix ultimately associated with loss of glomerular 22 CSAKY AND COUSINS M ELM M RPE RPE BLD GS AMD Figure 6 Electron micrographs from glomerulosclerosis and geographic atrophy from age-related macular degeneration (AMD) showing appearance of excessive extracellular material and cellular loss.
However, bystander recruitment of T cells occurs in many other forms of pathological neovascularization and wound healing. Nonspeciﬁc ampliﬁcation mechanisms may also play a role in AMD. Recently, several groups have identiﬁed complement components in drusen (22,182). Fragments of C5 and the MAC were identiﬁed in most specimens, and C3 was present in some. The activation pathway remains unknown. The RPE express speciﬁc and nonspeciﬁc complement inhibitors such as decay accelerating factor and vitronectin to suggest intrinsic defense mechanisms to prevent against complementmediated injury (183).