Specialized Pro-resolving Mediators and Omega-3s

August 5, 2019 • 3 min read

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 [1] [2].

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 [1].

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.[1]

Lipid mediators, cytokines, chemokines, and complement components stimulate chemotaxis to move neutrophils into necessary tissues to break down and neutralize invaders through phagocytosis.[1]

Phase 2 (the resolution phase): Receptor antagonists resolve inflammation.

SPMs prevent neutrophils from continuing to enter tissues and promote macrophages to clear cellular debris.[1]

When inflammation resolution fails, inflammation will become excessive and chronic.[1]

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. [1] Prostaglandins, along with leukotrienes, are produced from arachidonic acid (AA), and are necessary to activate the resolution phase of inflammation. [5] Aspirin and NSAIDs inhibit prostaglandin biosynthesis, which in turn may inhibit the activation of the resolution phase [1]

Phase 2 resolution:

Microparticles are membrane-derived vesicles produced by self-resolving exudates, and they have anti-inflammatory and pro-resolving capacities.[1] 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.[3] Activation of macrophages is an essential step towards the resolution of inflammation. [3]

Eosinophils are white blood cells specific to parasitic infections and allergic responses, and they support SPM production. [1]

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  1. Serhan, C.N., Pro-resolving lipid mediators are leads for resolution physiology. Nature, 2014. 510(7503): p. 92-101.
  2. Maderna, P. and C. Godson, Lipoxins: resolutionary road. Br J Pharmacol, 2009. 158(4): p. 947-59.
  3. Spite, M., J. Claria, and C.N. Serhan, Resolvins, specialized proresolving lipid mediators, and their potential roles in metabolic diseases. Cell Metab, 2014. 19(1): p. 21-36.
  4. Li, Y., et al., Plasticity of leukocytic exudates in resolving acute inflammation is regulated by MicroRNA and proresolving mediators. Immunity, 2013. 39(5): p. 885-98.
  5. Ricciotti, E. and G.A. FitzGerald, Prostaglandins and inflammation. Arterioscler Thromb Vasc Biol, 2011. 31(5): p. 986-1000.

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