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- W2918019780 abstract "Uncontrolled inflammation is a key player in the pathogenesis of a myriad of chronic diseases including rheumatoid arthritis. Research has focused on understanding the mediators that cause chronic inflammatory responses in order to treat these diseases, and predominantly aims to inhibit the synthesis or action of mediators that drive inflammation using drugs such as NSAIDs. SPMs, identified in recent years, are endogenous mediators that include the n-3-derived families resolvins, protectins, and maresins, as well as AA-derived (n-6) lipoxins, which play a key role in promoting resolution processes and are a key target for the development of therapeutics that promote resolution. Resolution is typically defined as a tightly regulated process that restores tissue homeostasis and prevents the development of chronic disease. Recent studies, however, have introduced an alternative model in which resolution is not the end of immune responses to infection/injury, but that there is immunological activity occurring after the resolution cascade is complete that alters the immune physiology of the affected tissue post-injury. Adapted homeostasis is an evolutionary trade-off, where the threat of secondary infection is a more desirable outcome than the development of immune activation in response to endogenous antigens. Understanding the events that occur during resolution and post-resolution to bring about adapted homeostasis may be key in discovering the origins of some chronic inflammatory and autoimmune diseases. Deciphering the origins of chronic inflammatory and autoimmune diseases remains elusive with reliance on therapies aimed at halting inflammation in its tracks. In recent years, an appreciation of targeting pathways by which inflammation is resolved has begun to rouse interest. Resolution of inflammation is driven by a complex set of mediators that regulate cellular events required to clear inflammatory cells from sites of infection or injury to restore tissue function. However, recent studies suggest that resolution is not the end of innate mediated immune responses to infection/injury. There is further immunological activity occurring after the resolution cascade is complete that alters the immune physiology of tissues, redefining what was once termed restorative homeostasis as adapted homeostasis. Deciphering the origins of chronic inflammatory and autoimmune diseases remains elusive with reliance on therapies aimed at halting inflammation in its tracks. In recent years, an appreciation of targeting pathways by which inflammation is resolved has begun to rouse interest. Resolution of inflammation is driven by a complex set of mediators that regulate cellular events required to clear inflammatory cells from sites of infection or injury to restore tissue function. However, recent studies suggest that resolution is not the end of innate mediated immune responses to infection/injury. There is further immunological activity occurring after the resolution cascade is complete that alters the immune physiology of tissues, redefining what was once termed restorative homeostasis as adapted homeostasis. multiple vesicles formed by fragmentation of the cell during apoptosis. antibodies produced by the immune system that are directed against one or more of the individuals own proteins. proteins released by immune cells that mediate the function and behaviour neighbouring cells during steady state and inflammation. removal of effete, mainly apoptotic cells, by professional phagocytes, especially macrophages. a group of extracellular matrix proteins responsible for the degradation of proteins such as collagen during normal tissue turnover. They also participate in several other physiological processes such as bone remodelling, angiogenesis, immunity, and wound healing. heterogeneous group of immune cells of the myeloid lineage characterised by the immature state and ability to supress T cell responses. large, extracellular, web-like structures composed of cytosolic and granule proteins that are assembled on a scaffold of decondensed chromatin. NETs released from neutrophils function to trap, neutralise, and kill a variety of extracellular pathogens. family of lipid mediators generated by the action of cyclooxygenase on a 20-carbon unsaturated fatty acid, AA, which modulate cell function during inflammation and resolution. lipid mediators derived from the ω-3 essential fatty acids eicosapentaenoic acid and docosahexaenoic acid, which can promote/accelerate inflammatory resolution. homeostatic process involved in the maintenance of an internal steady state within a defined tissue of an organism, including control of cellular proliferation and death and control of metabolic function. ligand found on the surface of fungi. It binds to TLR2 and dectin receptors." @default.
- W2918019780 created "2019-03-02" @default.
- W2918019780 creator A5012953668 @default.
- W2918019780 creator A5024695885 @default.
- W2918019780 date "2019-03-01" @default.
- W2918019780 modified "2023-10-16" @default.
- W2918019780 title "Is Resolution the End of Inflammation?" @default.
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