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Endogenous lipid mediators in the resolution of airway inflammation

Pulmonary and Critical Care Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.

CORRESPONDENCE: B. D. Levy, Pulmonary and Critical Medicine, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA. Fax: 1 6172324623. E-mail: blevy{at}partners.org

Keywords: Acute respiratory distress syndrome, asthma, inflammation, lipoxins, mediators, resolution

Received: January 16, 2007
Accepted June 15, 2007

Acute inflammation in the lung is fundamentally important to host defence, but chronic or excessive inflammation leads to several common respiratory diseases, including asthma and acute respiratory distress syndrome.

The resolution of inflammation is an active process. In health, events at the onset of acute inflammation establish biosynthetic circuits for specific chemical mediators that later serve as agonists to orchestrate a return to tissue homeostasis. In addition to an overabundance of pro-inflammatory stimuli, pathological inflammation can also result from defects in resolution signalling.

The understanding of anti-inflammatory, pro-resolution molecules and their counter-regulatory signalling pathways is providing new insights into the molecular pathophysiology of lung disease and opportunities for the design of therapeutic strategies.

In the present review, the growing family of lipid mediators of resolution is examined, including lipoxins, resolvins, protectins, cyclopentenones and presqualene diphosphate. Roles are uncovered for these compounds, or their structural analogues, in regulating airway inflammation.