Research summary
Specialized pro-resolving mediators and the active resolution of inflammation define this work. A 1987 Science paper synthesized the biosynthesis and biological effects of leukotrienes and lipoxins, describing how arachidonic acid released from membrane phospholipids upon cell stimulation is converted by 5-lipoxygenase (which also has LTA4 synthetase activity) to the unstable epoxide leukotriene A4 and then to LTB4 by leukotriene A4 hydrolase or to the cysteinyl leukotrienes by glutathione conjugation; the paper also described the transcellular biosynthesis of lipoxins from leukocyte鈥損latelet interactions via 5-lipoxygenase and 12-lipoxygenase coupling, framing eicosanoid biology as a multicellular process [1]. A 2000 Journal of Experimental Medicine paper identified novel anti-inflammatory mediators derived from omega-3 eicosapentaenoic and docosahexaenoic acids via aspirin-acetylated cyclooxygenase-2 and transcellular processing by leukocyte lipoxygenases, providing the biochemical foundation for the resolvin series and explaining at the molecular level how aspirin can be both anti-inflammatory and pro-resolution [4]. A 2002 paper formally introduced the resolvins, showing that lipidomic profiling of resolution-phase inflammatory exudates from mouse air-pouch models identifies the E- and D-series resolvins as endogenous lipid mediators that actively limit polymorphonuclear leukocyte infiltration and promote tissue homeostasis at nanomolar concentrations [2]. A 2007 FASEB Journal consensus piece formalized the terminology of inflammation resolution as a programmed active process distinct from passive cytokine-and-chemokine decay, and defined standardized quantitative indices (resolution interval Ri, R index) to compare experimental models across laboratories [5]. A 2018 Journal of Clinical Investigation review on resolvins in inflammation organized the broader pro-resolving superfamily including resolvins, protectins, maresins, and lipoxins, summarized their G-protein-coupled receptor pharmacology, and reviewed therapeutic implications across chronic inflammatory and infectious disease including periodontitis, asthma, and infection [3]. The recurring methodological thread is the use of lipidomic and bioassay-guided isolation to identify endogenous mediators whose action distinguishes active resolution from passive decay of inflammation.
Recent publications
- Resolving inflammation: dual anti-inflammatory and pro-resolution lipid mediatorsDOI
- Pro-resolving lipid mediators are leads for resolution physiologyDOI
- Resolution of inflammation: the beginning programs the endDOI
- Leukotrienes and Lipoxins: Structures, Biosynthesis, and Biological EffectsDOI
- ResolvinsDOI
- Lipid mediator class switching during acute inflammation: signals in resolutionDOI
- Resolvins in inflammation: emergence of the pro-resolving superfamily of mediatorsDOI
- Novel Functional Sets of Lipid-Derived Mediators with Antiinflammatory Actions Generated from Omega-3 Fatty Acids via Cyclooxygenase 2鈥揘onsteroidal Antiinflammatory Drugs and Transcellular ProcessingDOI
- Resolvin E1 and protectin D1 activate inflammation-resolution programmesDOI
- Resolution of in flammation: state of the art, definitions and termsDOI
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Email Charles N. Serhan 6-12 months before your application deadline. Read several recent papers and reference specific work in your message. Use our how to email a Japanese professor guide for the proven email structure.
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External profiles
- ORCID: https://orcid.org/0000-0003-4627-8545
- OpenAlex: openalex.org
Profile compiled from public sources (Researchmap, OpenAlex, Kyushu University faculty directory). Last refreshed 2026-05. Report incorrect information.