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Inflammopharmacology
Erschienen in:

18.01.2022 | Commentary

Mechanism by which immune complexes are deposited in hosts tissue

verfasst von: Isaac Ginsburg, Mark Feldman

Erschienen in: Inflammopharmacology | Ausgabe 1/2022

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Abstract

We offer an explanation how immune complexes are deposited in tissues of auto-immune disorders in humans. These disorders are characterized by the accumulation in tissues of large numbers of neutrophils, which can shed out long extracellular traps (NETs) rich in a nucleosome and in highly opsonic poly cations, histone, LL37, defensins and elastase possessing properties similar to antibodies. These can bind by strong electrostatic forces to negatively charged domains in immune globulins, thus facilitating their deposition and internalization by tissue cells. However, the main cause for tissue damage in auto-immune patients is inflicted by the plethora of toxic pro-inflammatory agents released by activated neutrophils. To ameliorate tissue damage and the cytokine storms, it is recommended to administer to patients highly anionic heparins accompanied by steroids, methotrexate, colchicine, copaxone, and also by additional agents which retarded neutrophil functions.
Literatur
Brinkmann V, Reichard U, Goosmann C, Fauler B, Uhlemann Y, Weiss DS, Weinrauch Y, Zychlinsky A (2004) Neutrophil extracellular traps kill bacteria. Science 303:1532–1535CrossRef
Chatfield SM, Thieblemont N, Witko-Sarsat V (2018) Expanding neutrophil horizons: new concepts in inflammation. J Innate Immun 10:422–431CrossRef
Chu F, Shi M, Zheng C, Shen D, Zhu J, Zheng X, Cui L (2018) The roles of macrophages and microglia in multiple sclerosis and experimental autoimmune encephalomyelitis. J Neuroimmunol 318:1–7CrossRef
Cromartie WJ, Craddock JG, Schwab JH, Anderle S, Yang C-H (1977) Arthritis in rats after systemic injection of streptococcal cells or cell walls. J Exp Med 146:1585–1602CrossRef
D’Elia RV, Harrison K, Oyston PC, Lukaszewski RA, Clark GC (2013) Targeting the “cytokine storm” for therapeutic benefit. Clin Vaccine Immunol 20:319–327CrossRef
Dalldorf FG, Cromartie WJ, Anderle SK, Clark RL, Schwab JH (1980) The relation of experimental arthritis to the distribution of streptococcal cell wall fragments. Am J Pathol 100:383PubMedPubMedCentral
Fox A, Schwab J, Cochran T (1980) Muramic acid detection in mammalian tissues by gas-liquid chromatography-mass spectrometry. Infect Immun 29:526–531CrossRef
Ginsburg I (1987) Cationic polyelectrolytes: a new look at their possible roles as opsonins, as stimulators of respiratory burst in leukocytes, in bacteriolysis, and as modulators of immune-complex diseases (a review hypothesis). Inflammation 11:489–515CrossRef
Ginsburg I (1998) Could synergistic interactions among reactive oxygen species, proteinases, membrane-perforating enzymes, hydrolases, microbial hemolysins and cytokines be the main cause of tissue damage in infectious and inflammatory conditions? Med Hypotheses 51:337–346CrossRef
Ginsburg I (2002a) The role of bacteriolysis in the pathophysiology of inflammation, infection and post-infectious sequelae. APMIS 110:753–770CrossRef
Ginsburg I (2002b) Role of lipoteichoic acid in infection and inflammation. Lancet Infect Dis 2:171–179CrossRef
Ginsburg I, Kohen R (1995a) Invited review: cell damage in inflammatory and infectious sites might involve a coordinated “cross-talk” among oxidants, microbial haemolysins and ampiphiles, cationic proteins, phospholipases, fatty acids, proteinases and cytokines (an overview). Free Radical Res 22:489–517CrossRef
Ginsburg I, Kohen R (1995b) Synergistic effects among oxidants, membrane-damaging agents, fatty acids, proteinases, and xenobiotics: killing of epithelial cells and release of arachidonic acid. Inflammation 19:101–118CrossRef
Ginsburg I, Koren E (2018) Bacteriolysis–a mere laboratory curiosity? Crit Rev Microbiol 44:609–618CrossRef
Ginsburg I, Sela MN, Morag A, Ravid Z, Duchan Z, Ferne M, Rabinowitz-Bergner S, Thomas PP, Davies P, Niccols J (1981) Role of leukocyte factors and cationic polyelectrolytes in phagocytosis of group a streptococci and Candida albicans by neutrophils, macrophages, fibroblasts and epithelial cells. Inflammation 5:289–312CrossRef
Ginsburg I, Mor N, Resnick M, Bercovier H (1986) Polycationic agent facilitates endocytosis of microorganisms by amoebae. Eur J Cell Biol Suppl 41:130–133
Ginsburg I, Misgav R, Pinson A, Varani J, Ward P, Kohen R (1992) Synergism among oxidants, proteinases, phospholipases, microbial hemolysins, cationic proteins, and cytokines. Inflammation 16:519–538CrossRef
Ginsburg I, Mitra RS, Gibbs DF, Varani J, Kohen R (1993) Killing of endothelial cells and release of arachidonic acid. Inflammation 17:295–319CrossRef
Ginsburg I, Ward PA, Varani J (1999) Can we learn from the pathogenetic strategies of group A hemolytic streptococci how tissues are injured and organs fail in post-infectious and inflammatory sequelae? FEMS Immunol Med Microbiol 25:325–338CrossRef
Ginsburg I, Rozenstein-Tsalkovich L, Koren E, Rosenmann H (2011) The herbal preparation padma® 28 protects against neurotoxicity in PC 12 cells. Phytother Res 25:740–743CrossRef
Ginsburg I, Korem M, Koren E, Varani J (2019) Pro-inflammatory agents released by pathogens, dying host cells, and neutrophils act synergistically to destroy host tissues: a working hypothesis. J Inflamm Res 12:35CrossRef
Hubner G, Voigt W, Schlumberger H, Ginsburg I (1985) Poly-L-arginine opsonizes nuclei for phagocytosis by mouse fibroblasts. IRCS Med Sci Biochem 13:934–935
Kaplan MJ (2013) Role of neutrophils in systemic autoimmune diseases. Arthritis Res Ther 15:1–9CrossRef
Li X, Ma X (2017) The role of heparin in sepsis: much more than just an anticoagulant. Br J Haematol 179:389–398CrossRef
Németh T, Mócsai A (2012) The role of neutrophils in autoimmune diseases. Immunol Lett 143:9–19CrossRef
Robak E, Robak T (2012) Novel and emerging drugs for systemic lupus erythematosus: mechanism of action and therapeutic activity. Curr Med Chem 19:438–453CrossRef
Smith JA (1994) Neutrophils, host defense, and inflammation: a double-edged sword. J Leukoc Biol 56:672–686CrossRef
van Bruggen MC, Walgreen B, Rijke TP, Corsius MJ, Assmann KJ, Smeenk RJ, van Dedem GW, Kramers K, Berden JH (1996) Heparin and heparinoids prevent the binding of immune complexes containing nucleosomal antigens to the GBM and delay nephritis in MRL/lpr mice. Kidney Int 50:1555–1564CrossRef
Warren J, Ward P, Johnson K, Ginsburg I (1987) Modulation of acute immune complex-mediated tissue injury by the presence of polyionic substances. Am J Pathol 128:67PubMedPubMedCentral
Wecke J, Lahav M, Ginsburg I, Giesbrecht P (1982) Cell wall degradation of Staphylococcus aureus by lysozyme. Arch Microbiol 131:116–123CrossRef
Wildhagen KC, der García Frutos P, Reutelingsperger CP, Schrijver R, Aresté C, Ortega-Gómez A, Deckers NM, Hemker HC, Soehnlein O, Nicolaes GA (2014) Nonanticoagulant heparin prevents histone-mediated cytotoxicity in vitro and improves survival in sepsis. Blood J Am Soc Hematol 123:1098–1101
Woodberry T, Bouffler SE, Wilson AS, Buckland RL, Brüstle A (2018) The emerging role of neutrophil granulocytes in multiple sclerosis. J Clin Med 7:511CrossRef
Xu J, Zhang X, Pelayo R, Monestier M, Ammollo CT, Semeraro F, Taylor FB, Esmon NL, Lupu F, Esmon CT (2009) Extracellular histones are major mediators of death in sepsis. Nat Med 15:1318–1321CrossRef
Yang H, Biermann MH, Brauner JM, Liu Y, Zhao Y, Herrmann M (2016) New insights into neutrophil extracellular traps: mechanisms of formation and role in inflammation. Front Immunol 7:302PubMedPubMedCentral
Metadaten
Titel
Mechanism by which immune complexes are deposited in hosts tissue
verfasst von
Isaac Ginsburg
Mark Feldman
Publikationsdatum
18.01.2022
Verlag
Springer International Publishing
Erschienen in
Inflammopharmacology / Ausgabe 1/2022
Print ISSN: 0925-4692
Elektronische ISSN: 1568-5608
DOI
https://doi.org/10.1007/s10787-021-00910-y

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