Transcriptional Regulation of Inflammatory Pain and Hyperalgesia: NF-kB as a Lynchpin and Master Regulator.
The milieu and array of inflammatory cells and inflammatory mediators are crucially involved in the genesis, persistence and severity of pain following trauma, infection or nerve injury [1]. The mechanisms and pathways mediating pain and nociception (hyperalgesia) are transcriptionally regulated. The transcriptional mediator nuclear factor (NF)-κB plays a major role in regulating inflammatory responses, ostensibly via the control of gene expression/suppression. An association has recently emerged to establish a possible link between NF-kB and pain/nociception, purportedly through the regulation of the inflammatory loop and the secretion (biosynthesis) of pro-inflammatory mediators.
Dr John Haddad provides an overview of the role of the gene encoded immune activated inflammatory amplifier in terms of persistent and debilitating pain syndromes. NFκB can be down regulated with the use of specific nutritional concentrates and dietary recommendations have the potential to influence this gene expression. Presented in SciTopics
Key Words: anti-inflammatory, cytokines, Inflammation, Pain, Immune system
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Keywords:anti inflammatory, cytokines, immune, inflammation, pain
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The immune system is prone to the same grave misfortunes as any defense system handling weapons: collateral damage that comes with the destruction of the enemy on one’s own territory and friendly fire due to mistaken identity. Whereas the collateral damage is the price we pay for clearance of infections, autoimmunity is a pathological process. Nevertheless, the effector mechanisms involved in both processes are the same. Whether environment can be a cause, a trigger or an amplifier of an autoimmune disease are questions that are being intensively investigated.
