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A Novel Hypothetical Approach to Explain the Mechanisms of Pathogenicity of Rheumatic Arthritis. | LitMetric

AI Article Synopsis

  • Rheumatoid arthritis (RA) is a chronic autoimmune disorder that leads to inflammation and damage of joints, muscles, and surrounding tissues through the accumulation of immune cells like neutrophils and macrophages.
  • Key mechanisms involve the release of toxic substances from activated neutrophils and the deposition of auto-antibodies in the joints via interactions with cationic histones released during a process known as NETosis.
  • Potential treatments to help mitigate tissue damage include the use of highly anionic heparins, which can counteract cationic histone activity, alongside traditional anti-inflammatory drugs like steroids and methotrexate.

Article Abstract

The autoimmune disorder rheumatoid arthritis (RA) is a relapsing and chronic inflammatory disease that affects the synovial cells, cartilage, bone, and muscle. It is characterised by the accumulation of huge numbers of polymorphonuclear neutrophils (PMNs) and macrophages in the synovia. Auto-antibodies are deposited in the joint via the activity of highly cationic histones released from neutrophil extracellular traps (NETs) in a phenomenon termed NETosis. The cationic histones function as opsonic agents that bind to negatively charged domains in autoantibodies and complement compounds via strong electrostatic forces, facilitating their deposition and endocytosis by synovial cells. However, eventually the main cause of tissue damage is the plethora of toxic pro-inflammatory substances released by activated neutrophils recruited by cytokines. Tissue damage in RA can also be accompanied by infections which, upon bacteriolysis, release cell-wall components that are toxic to tissues. Some amelioration of the damaged cells and tissues in RA may be achieved by the use of highly anionic heparins, which can neutralize cationic histone activity, provided that these polyanions are co-administrated with anti-inflammatory drugs such as steroids, colchicine, or methotrexate, low molecular weight antioxidants, proteinase inhibitors, and phospholipase A2 inhibitors.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8369279PMC
http://dx.doi.org/10.31138/mjr.32.2.112DOI Listing

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