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Inflammatory cytokines play a role in initiating the inflammatory response and to regulate the host defence against pathogens mediating the innate immune response. [4] Some inflammatory cytokines have additional roles such as acting as growth factors. [5] Pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α also trigger pathological pain ...
Cytokines also play a role in anti-inflammatory pathways and are a possible therapeutic treatment for pathological pain from inflammation or peripheral nerve injury. [22] There are both pro-inflammatory and anti-inflammatory cytokines that regulate this [clarification needed] pathway.
Other chemokines are inflammatory and are released from a wide variety of cells in response to bacterial infection, viruses and agents that cause physical damage such as silica or the urate crystals that occur in gout. Their release is often stimulated by pro-inflammatory cytokines such as interleukin 1.
Pro-inflammatory cytokine secreted by macrophages in response to pathogen-associated molecular patterns (PAMPs); pro-inflammatory cytokine secreted by adipocytes, especially in obesity; anti-inflammatory myokine secreted by skeletal muscle cells in response to exercise.
Interleukin 6 (IL-6) is an interleukin that acts as both a pro-inflammatory cytokine and an anti-inflammatory myokine. In humans, it is encoded by the IL6 gene. [5] In addition, osteoblasts secrete IL-6 to stimulate osteoclast formation. Smooth muscle cells in the tunica media of many blood vessels also produce IL-6 as a pro-inflammatory cytokine.
GAGs bind to cytokines and regulate cell recruitment, inflammation, and tissue remodeling by delivering cytokines to the extracellular matrix. [ 9 ] [ 10 ] Binding studies suggest GAGs have a natural affinity for cytokines, and cytokine binding to GAGs is mediated by nonspecific electrostatic interactions between positively charged domains on ...
TNF amplifies and prolongs the inflammatory response by activating other cells to release interleukin-1 (IL-1), high mobility group B1 and other cytokines. [4] These inflammatory cytokine responses confer protective advantages to the host at the site of bacterial infection. A “beneficial” inflammatory response is limited, resolves in 48 ...
They, too, activate human granulocytes (neutrophils, eosinophils and basophils) which can lead to acute neutrophilic inflammation. They also induce the synthesis and release of other pro-inflammatory cytokines such as interleukin 1 (IL-1), IL-6 and TNF-α from fibroblasts and macrophages.
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