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Number of results
2001 | 49 | 3 | 177-188

Article title

Lipoxins and aspirin-triggered 15-epi-lipoxins are endogenous components of anti-inflammation: emergence of the counterregulatory side

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Languages of publication

EN

Abstracts

EN
Eicosanoids are known to play important roles in cell-cell communications and as intracellular signals that are critical components of multi-cellular responses such as acute inflammation and reperfusion injury. Recent findings have given rise to several new concepts that are reviewed here regarding the generation of eicosanoids and their impact in inflammation. Lipoxins (LX) are trihydroxytetraene-containing eicosanoids that can be generated within the vascular lumen during platelet-leukocyte interactions and at mucosal surfaces via leukocyte-epithelial cell interactions. During these cell-cell interactions, transcellular biosynthetic pathways are used as major LX biosynthetic routes, and thus, in humans, LX are formed in vivo during multi-cellular responses such as inflammation, atherosclerosis, and in asthma. This branch of the eicosanoid cascade generates specific tetraene-containing products that serve as stop signals, in that they regulate key steps in leukocyte trafficking and prevent leukocyte-mediated acute tissue injury. Of interest here are recent results indicating that aspirin's mechanism of action also involves the triggering of novel carbon 15 epimers of LX or 15-epi-LX that mimic the bioactions of native LX. Here, an overview of these recent developments is presented, with a focus on the cellular and molecular interactions of these novel antiinflammatory lipid mediators.

Contributors

author

References

Document Type

REVIEW

Publication order reference

Ch. N. Serhan, Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA

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YADDA identifier

bwmeta1.element.element-from-psjc-db0ffe94-81a6-3ec4-9b2f-2708cc44651f
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