Anti-inflammatory circuitry: Lipoxin, aspirin-triggered lipoxins and their receptor ALX

Nan Chiang, Makoto Arita, Charles N. Serhan

Research output: Contribution to journalArticle

189 Citations (Scopus)

Abstract

Endogenous chemical mediators or autacoids play key roles in controlling inflammation and its programmed resolution. Among them, it is known that lipoxins (LX) and aspirin-triggered LX (ATL) evoke bioactions in a range of physiologic and pathophysiologic processes and serve as endogenous lipid/chemical mediators that stop neutrophilic infiltration and initiate resolution. LXA4, ATL and their metabolic stable analogs elicit cellular responses and regulate PMN in vivo via interacting with their specific receptor, namely ALX. ALX is the first cloned and identified lipoxygenase-derived eicosanoid receptor with cell type-specific signaling pathways. Also, ALX could regulate PMN by interacting with each class of ligands (lipid vs. peptide) within specific phases of an inflammatory response. Together LX, ATL and ALX may provide new opportunities to design "resolution-targeted" therapies with high degree of precision in controlling inflammation. In this chapter, we give an overview and update of the current actions for LX and ATL, the identification of ALX and their novel anti-inflammatory and pro-resolving signals.

Original languageEnglish
Pages (from-to)163-177
Number of pages15
JournalProstaglandins Leukotrienes and Essential Fatty Acids
Volume73
Issue number3-4
DOIs
Publication statusPublished - 2005 Jan 1
Externally publishedYes

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology

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