Lipoxin signaling in neutrophils and their role in periodontal disease.
Endogenous molecules involved in counterregulation of inflammatory responses provide an opportunity to explore new therapeutic approaches based on manipulation of new pathways that may reduce the possibility of unwanted toxic side effects. Lipoxins (LX) are trihydroxytetraene-containing eicosanoids that are generated within the vascular lumen during cell-cell interactions or at mucosa through leukocyte-epithelial cell interactions. Transcellular biosynthetic pathways are the major lipoxin biosynthetic routes where LX are formed in vivo during inflammation and serve as "stop signals" that regulate key steps in leukocyte trafficking. In this review, recent findings in lipoxin generation, impact on the resolution of acute inflammation, and organ protection from neutrophil-mediated injury are presented. Periodontitis, specifically localized aggressive periodontitis, which is recognized as an example of neutrophil-mediated tissue injury, is discussed as a disease model where LX and other endogenous pro-resolution pathway mediators could have potential value.
Department of Periodontology and Oral Biology, Boston University Goldman School of Dental Medicine, 100 East Newton Street, G-05, Boston, MA 02118, USA.
Alpdogan
A
Kantarci
Thomas E
TE
Van Dyke
D000818:Animals; D000893:Anti-Inflammatory Agents; D016718:Arachidonic Acid / Q000378:metabolism*; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D044045:Lipoxins / Q000502:physiology*; D009504:Neutrophils / Q000502:physiology*; D010518:Periodontitis / Q000378:metabolism / Q000503:physiopathology*; D015398:Signal Transduction / Q000502:physiology*
D000893:Anti-Inflammatory Agents; D018836:Inflammation Mediators; D044045:Lipoxins; D016718:Arachidonic Acid