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The Chemistry and Biology of Lipooligosaccharides: The Endotoxins of Bacteria of the Respiratory and Genital Mucosae
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
J. McLeod Griffiss, Herman Schneider
The terminal Gal residues of human glycoconjugates often are substituted with sialic acid (also called N-acetylneuraminic acid or NANA). Sialylation affects many biological functions. Sialylation of cell membrane glycoconjugates aborts assemblage of the complement membrane attack complex and prevents its lysis of cells (66–68). It also protects cells from recognition and clearance by antibody and complement-independent immune mechanisms, interferes with ligand binding to receptors on phagocytic cells, and prevents clearance of circulating glycoconjugates by hepatocytes.
Multiple sclerosis
Published in Jacques Corcos, David Ginsberg, Gilles Karsenty, Textbook of the Neurogenic Bladder, 2015
Jaspreet Singh Parihar, Hari S.G.R. Tunuguntla, Line Leboeuf, Angelo E. Gousse
The association of T cells and antigen in the CNS activates B lymphocyte cells, which subsequently differentiate into antibody-secreting plasma cells. The potential for damage from those antibodies resides in the opsonization of the autoimmune target and the activation of the complement membrane attack complex; all of these phenomena subsequently cause damage to the myelin and the myelin oligodendrocyte glycoprotein (MOG).13 Antibodies to MOG have been demonstrated within human MS lesions.14
Host Defenses Against Prototypical Intracellular Protozoans, the Leishmania
Published in Peter D. Walzer, Robert M. Genta, Parasitic Infections in the Compromised Host, 2020
Richard D. Pearson, Mary E. Wilson
Both immune and nonimmune human serum can kill promastigotes (89,91, 104-112). Promastigotes of many Leishmania species have been shown to be susceptible to killing by the complement membrane attack complex (C5b-C9). The mechanism of complement activation varies: L. major and L. enriettii promastigotes activate complement via the alternative pathway (89), while L. donovani promastigotes also activate it via the classical pathway (91). Fixation of complement on the parasite surface results in opsonization with C3b and then C3bi and death of the organism if the membrane attack complex is activated. Stationary-phase promastigotes are more resistant to complementmediated killing than logarithmic-stage parasites (112). In the L. major system, log-phase organisms activate complement with deposition of covalently bound C3b on their surface. They are killed by the membrane attack complex. Stationary-phase infective promastigotes bind C3b but not covalently and are not killed (113). Developmentally regulated LPG appears to be a major C3 receptor on both types of promastigotes (113). When polymorphonuclear leukocytes are present, ingestion of complement-opsonized promastigotes may result in parasite death (97). Conversely, complement-mediated ingestion of promastigotes by oxidatively weak macrophages may facilitate entry of the parasite into a sanctuary where it can convert to its amastigote form. Activation of complement by promastigotes may also result in macrophage chemotaxis toward the parasite (114). It has also been postulated that promastigotes may be inoculated by sandflies into the skin at a site where complement is not active or, more likely, that proteases in sandfly saliva might inactivate complement, protecting the parasite from the lethal effects of the membrane attack complex.
Association of Systemic Inflammatory Factors with Progression to Advanced Age-related Macular Degeneration
Published in Ophthalmic Epidemiology, 2022
Brandie D. Wagner, Jennifer L. Patnaik, Alan G. Palestine, Ashley A. Frazer-Abel, Rebecca Baldermann, V. Michael Holers, Marc T. Mathias, Naresh Mandava, Anne M. Lynch
The PC that was most associated with age was positively weighted by CRP, IL8, IL6 and TNFα, all of which were similarly associated with age using PCA in another study.36 Previous studies focusing on understanding changes in the inflammatory system associated with age (inflamm-aging) have shown that there are simultaneous changes in both pro- and anti-inflammatory markers.35,36 Our analyses similarly found variations in analyte levels with age not represented by a simple increase in all markers, or a change in the relative balance between pro- and anti-inflammatory markers, but rather a more complex relationship. Previous studies have shown an association between age and systemic risk factors with development of AMD,7,10,47 and a broad impact of systemic inflammation on the risk of other chronic diseases.35,36 Further findings indicate complement components, as constituents of drusen,23 markers of complement activation in the aqueous humor,48 and the complement membrane attack complex in the choriocapillaris,49,50 as well as, a role for the complement system and other inflammatory pathways in iAMD after adjusting for age.32,34 In combination, these findings suggest that systemic inflammation could contribute to an increased risk of AMD despite the longstanding notion that AMD is a local disease with links to local inflammatory events.
Nanotechnology: revolutionizing the delivery of drugs to treat age-related macular degeneration
Published in Expert Opinion on Drug Delivery, 2021
The role of chronic disposition of the complement membrane attack complex (MAC) in both dry and wet AMD is a hot topic in AMD research as high levels of MAC lead to cell death. CD 59 is a membrane-bound protective protein that is a natural inhibitor of MAC. This has prompted the investment and search for therapeutic strategies for MAC inhibition [142]. The first human gene therapy clinical trial (NCT03144999) has completed recruitment to evaluate the safety of a single injection of AAVCAGsCD59 (a soluble form of CD59) designed to protect the retinal cells by inhibiting MAC formation. Since it is given as intra-vitreal injection, the role of nanotechnology to improve the site-specific delivery would be an exciting next step.