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Age-related macular degeneration in the aspect of chronic low-grade inflammation (pathophysiological
Małgorzata Nita1, Andrzej Grzybowski2, Francisco J Ascaso3
1Domestic and Specialized Medicine Centre "Dilmed", Bohaterów Monte Cassino 3, 40-231 Katowice, Poland.
Abstract:
The products of oxidative stress trigger chronic low-grade inflammation (pathophysiological parainflammation) process in AMD patients. In early AMD, soft drusen contain many mediators of chronic low-grade inflammation such as C-reactive protein, adducts of the carboxyethylpyrrole protein, immunoglobulins, and acute phase molecules, as well as the complement-related proteins C3a, C5a, C5, C5b-9, CFH, CD35, and CD46. The complement system, mainly alternative pathway, mediates chronic autologous pathophysiological parainflammation in dry and exudative AMD, especially in the Y402H gene polymorphism, which causes hypofunction/lack of the protective complement factor H (CFH) and facilitates chronic inflammation mediated by C-reactive protein (CRP). Microglial activation induces photoreceptor cells injury and leads to the development of dry AMD. Many autoantibodies (antibodies against alpha beta crystallin, alpha-actinin, amyloid, C1q, chondroitin, collagen I, collagen III, collagen IV, elastin, fibronectin, heparan sulfate, histone H2A, histone H2B, hyaluronic acid, laminin, proteoglycan, vimentin, vitronectin, and aldolase C and pyruvate kinase M2) and overexpression of Fcc receptors play role in immune-mediated inflammation in AMD patients and in animal model. Macrophages infiltration of retinal/choroidal interface acts as protective factor in early AMD (M2 phenotype macrophages); however it acts as proinflammatory and proangiogenic factor in advanced AMD (M1 and M2 phenotype macrophages).
Insights
Oxidative stress drives chronic inflammation in age-related macular degeneration (AMD). The complement system and autoantibodies contribute to AMD pathogenesis, while macrophage roles shift from protective to inflammatory in advanced stages.
Area of Science:
- Ophthalmology
- Immunology
- Pathophysiology
Background:
- Oxidative stress products initiate chronic low-grade inflammation (pathophysiological parainflammation) in age-related macular degeneration (AMD) patients.
- Soft drusen in early AMD contain numerous inflammation mediators, including acute phase molecules and complement system proteins.
- The complement system's alternative pathway is implicated in chronic inflammation in both dry and exudative AMD, particularly with the Y402H gene polymorphism affecting complement factor H (CFH).
Purpose of the Study:
- To elucidate the role of oxidative stress, inflammation, and immune responses in the pathogenesis of age-related macular degeneration (AMD).
- To investigate the involvement of the complement system and autoantibodies in AMD development and progression.
- To understand the dual role of macrophages in different stages of AMD.
Main Methods:
- Analysis of inflammation mediators within soft drusen in early AMD.
- Investigation of complement system activation, focusing on the alternative pathway and Y402H polymorphism.
- Examination of autoantibody profiles and Fc receptor expression in AMD patients and animal models.
- Assessment of macrophage infiltration and phenotypes at the retinal/choroidal interface in early and advanced AMD.
Main Results:
- Products of oxidative stress trigger chronic low-grade inflammation in AMD.
- The complement system, particularly the alternative pathway and CFH polymorphism, drives inflammation in AMD.
- Microglial activation contributes to photoreceptor injury and dry AMD development.
- Numerous autoantibodies and Fc receptor overexpression are involved in immune-mediated inflammation in AMD.
- Macrophages exhibit distinct roles, being protective in early AMD but proinflammatory and proangiogenic in advanced AMD.
Conclusions:
- Chronic inflammation, driven by oxidative stress and the complement system, is central to AMD pathogenesis.
- Immune responses, including autoantibodies and specific macrophage phenotypes, significantly influence AMD progression.
- Targeting inflammatory pathways and understanding immune cell dynamics may offer therapeutic strategies for AMD.
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