Anti-Inflammatory Signaling Molecules are endogenous biochemical messengers, including certain specialized pro-resolving mediators (SPMs), regulatory cytokines, and hormones, that actively regulate and terminate the inflammatory response. Their presence and activity are essential for maintaining tissue homeostasis and preventing chronic, low-grade systemic inflammation, a primary driver of age-related decline and hormonal dysfunction. Optimizing the profile of these molecules is a core therapeutic strategy in managing overall metabolic and endocrine health. These molecules ensure that inflammation is a transient, self-limiting process.
Origin
The term combines concepts from immunology, specifically the study of cell signaling, and biochemistry, focusing on the molecular nature of these messengers. Cytokines and hormones have long been known as signaling molecules, but the emphasis on their active anti-inflammatory role highlights a critical shift toward understanding inflammation resolution as an actively regulated, vital process. This clinical focus evolved from recognizing the detrimental link between chronic, unresolved inflammation and widespread endocrine system dysfunction.
Mechanism
Anti-inflammatory signaling molecules operate by binding to specific cellular receptors on immune and non-immune cells, triggering intracellular cascades that actively inhibit pro-inflammatory gene transcription, such as NF-κB activation. They promote the clearance of cellular debris and the controlled resolution of the inflammatory site, facilitating a return to a non-inflamed, quiescent state. Hormones like cortisol and specific sex steroids also modulate immune cell function, directly contributing to this crucial regulatory mechanism by dampening excessive immune responses.
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