Specialized pro-resolving mediators (SPMs) exist at the heart of the physiological response vital for resolving inflammation. Inadequate inflammation resolution builds a foundation for a plethora of chronic conditions, and thus fully understanding and appreciating the role of SPMs in homeostasis is critical for addressing these conditions. SPMs are derived from omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), and they include resolvins, maresins, protectins, and lipoxins.
What Are SPMs?
Primarily, SPMs promote the resolution phase of inflammation, subsequently playing a role in host defense, organ protection, and tissue remodeling. SPMs initiate physiological changes at the inflammation site by 1) ending neutrophil infiltration and 2) promoting macrophage uptake of apoptotic cells  .
Secondarily, SPMs keep pro-inflammatory mediators (e.g. eicosanoids, chemokines, and cytokines) in check, regulate specific microRNA activity, and enhance microbial killing [3, 4].
Why Care About SPMs?
The resolution phase of inflammation prevents inflammation from turning into excessive chronic inflammation, leading to a variety of conditions like vascular disease, metabolic syndrome, and neurological diseases .
Phases of Inflammation
Phase 1 (the initiation phase): Pro-inflammatory lipid mediators derived from polyunsaturated omega-6 arachidonic acid (ARA) and various cytokines and chemokines initiate inflammation.
Lipid mediators, cytokines, chemokines, and complement components stimulate chemotaxis to move neutrophils into necessary tissues to break down and neutralize invaders through phagocytosis.
Phase 2 (the resolution phase): Receptor antagonists resolve inflammation.
SPMs prevent neutrophils from continuing to enter tissues and promote macrophages to clear cellular debris.
When inflammation resolution fails, inflammation will become excessive and chronic.
Other Important Players
Phase 1 initiation:
Prostaglandins and leukotrienes are eicosanoid pro-inflammatory lipid mediators important for vascular responses and neutrophils and monocytes exiting the circulation.  Prostaglandins, along with leukotrienes, are produced from arachidonic acid (AA), and are necessary to activate the resolution phase of inflammation.  Aspirin and NSAIDs inhibit prostaglandin biosynthesis, which in turn may inhibit the activation of the resolution phase 
Phase 2 resolution:
Microparticles are membrane-derived vesicles produced by self-resolving exudates, and they have anti-inflammatory and pro-resolving capacities. Microparticles also enhance macrophage clearing of debris during resolution and enhance SPM biosynthesis.
M2 Macrophages are pro-resolving white blood cells that support SPM production and engulf apoptotic neutrophils. Activation of macrophages is an essential step towards the resolution of inflammation. 
Eosinophils are white blood cells specific to parasitic infections and allergic responses, and they support SPM production.