Organizers: Charles N. Serhan, Harvard Medical School; George Zavoico, Cantor Fitzgerald
1:00 - 1:10 PM Introduction George Zavoico, Cantor Fitzgerald, New York, NY
1:10 - 1:50 PM "Resolvins and Protectins: Novel Lipid Mediators in Resolution of Inflammation" Charles N. Serhan, Harvard Medical School, Boston, MA
1:50 – 2:30 PM "Lipid Anti-Inflammatory Mediators and the Cystic Fibrosis Lung" Christopher Karp, Cincinnati Children's Hospital Medical Center and the University of Cincinnati College of Medicine, Cincinnati, OH
2:30 – 3:10 PM "Aspirin-Inhibited COX-2 Generates Resolvins that Promote the Resolution of Inflammation" Derek Gilroy, University College London, London, UK
3:10 – 3:40 PM Coffee Break
3:40 – 4:20 PM "Lipoxins and Regulation of Innate Immunity to Infection" Julio Aliberti, University of Cincinnati College of Medicine, Cincinnati, OH
4:20 – 5:00 PM "Synthetic Lipoxin Analogs: New Therapeutic Concepts in Inflammation, Allergy, and Gastroenterology" John F. Parkinson, Berlex Biosciences, Richmond, CAAbstract
Resolvins and Protectins: Novel Lipid Mediators in Resolution of Inflammation
Charles N. Serhan
Harvard Medical School
A well-integrated and controlled inflammatory response and its ending, i.e. resolution, is essential in health and disease. Our current research focuses on elucidating both the cellular and molecular events that govern resolution. This lecture will give an update and overview of recent advances from studies by the author and colleagues on the biosynthesis and actions of novel families of local acting anti-inflammatory lipid mediators coined resolvins and protectins that are produced from the omega-3 fatty acids (EPA and DHA). These previously unappreciated mediators were originally isolated from experimental murine models of acute inflammation captured during the natural spontaneous resolution phase. Specific members of these families possess stereospecific anti-inflammatory, proresolving, and protective properties. Since the resolvins and protectins in animal models control the duration and magnitude of inflammation, mapping of these resolution circuits provide new avenues for appreciating the molecular basis of many inflammatory diseases.
Lipid Anti-Inflammatory Mediators and the Cystic Fibrosis Lung
Cincinnati Children's Hospital Medical Center and the University of Cincinnati College of Medicine
Cystic fibrosis (CF), a lethal autosomal recessive disorder, is caused by mutations in the gene encoding the CF transmembrane conductance regulator (CFTR). The major clinical manifestations of CF include exocrine pancreatic insufficiency, male infertility, and chronic pulmonary disease, the latter being the main cause of morbidity and mortality. The CF airway is marked by chronic bacterial colonization and persistent neutrophilic inflammation. The end result is progressive, bronchiectatic destruction of the lung. Despite the insights afforded by the identification of CFTR in 1989, a clear understanding of the pathogenesis of lung disease in CF has remained elusive. The theoretical and experimental focus on CFTR as a regulator of epithelial ion transport has provided a compelling account of the pathogenesis of gastrointestinal disease in CF as well as of the genesis of such CF-associated phenomena as high sweat NaCl content. However, the examination of altered ion and water transport alone has failed to clearly illuminate the path from gene to pathogenesis in the CF airway.
The CF airway exhibits an aberrant proinflammatory diathesis. In additio