Inflammatory resolution is the active, programmed cessation of the acute inflammatory response and the return of the tissue to a state of homeostasis. It is not merely the passive dissipation of inflammation but a complex, coordinated biological process involving specialized pro-resolving mediators (SPMs). This process is crucial for preventing chronic inflammation, which is a key driver of many age-related and endocrine-related diseases, including insulin resistance and cardiovascular disease. A failure in inflammatory resolution, rather than an excess of inflammation itself, is increasingly recognized as a pathological feature.
Origin
While inflammation has been studied for centuries, the concept of active resolution as a distinct biological phase emerged in the early 21st century. Researchers identified novel lipid mediators derived from omega-3 fatty acids that actively signal the end of the inflammatory cascade, challenging the older view that inflammation simply faded away. The term formalizes the understanding that the body must actively shut down the immune response to prevent self-damage.
Mechanism
The mechanism is initiated by a “class switch” in the eicosanoid production pathway, moving from pro-inflammatory mediators like prostaglandins and leukotrienes to the production of specialized pro-resolving mediators (SPMs), such as resolvins, protectins, and maresins. These SPMs actively signal to immune cells, promoting the non-phlogistic clearance of apoptotic cells and cellular debris by macrophages, a process called efferocytosis. They also inhibit the further infiltration of pro-inflammatory cells, effectively silencing the inflammatory response and initiating tissue repair, thereby restoring functional integrity.
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