Lipid mediators in the resolution of inflammation - PubMed (original) (raw)

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Lipid mediators in the resolution of inflammation

Charles N Serhan et al. Cold Spring Harb Perspect Biol. 2014.

Abstract

Mounting of the acute inflammatory response is crucial for host defense and pivotal to the development of chronic inflammation, fibrosis, or abscess formation versus the protective response and the need of the host tissues to return to homeostasis. Within self-limited acute inflammatory exudates, novel families of lipid mediators are identified, named resolvins (Rv), protectins, and maresins, which actively stimulate cardinal signs of resolution, namely, cessation of leukocytic infiltration, counterregulation of proinflammatory mediators, and the uptake of apoptotic neutrophils and cellular debris. The biosynthesis of these resolution-phase mediators in sensu stricto is initiated during lipid-mediator class switching, in which the classic initiators of acute inflammation, prostaglandins and leukotrienes (LTs), switch to produce specialized proresolving mediators (SPMs). In this work, we review recent evidence on the structure and functional roles of these novel lipid mediators of resolution. Together, these show that leukocyte trafficking and temporal spatial signals govern the resolution of self-limited inflammation and stimulate homeostasis.

Copyright © 2015 Cold Spring Harbor Laboratory Press; all rights reserved.

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Figures

Figure 1.

Figure 1.

Lipid-mediator biosynthesis in exudate cell traffic in resolution of acute inflammation. Specialized proresolving mediators (SPMs) are generated during inflammation resolution and control the early events in acute inflammation such as edema formation, leukocyte trafficking, and functions (see text).

Figure 2.

Figure 2.

E-series resolvin biosynthesis and major function (see text for details).

Figure 3.

Figure 3.

D-series resolvin biosynthesis. The complete stereochemistry of RvD1, RvD2, and RvD3 is established (see Dalli et al. 2013a and text for further details).

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