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Lipoxin A4: a new direction in asthma therapy?

Asthma continues to be a common and significant disease with substantial medical and economic unmet needs despite current therapies. In view of this medical and social imperative, the pathobiology of asthma is an area of active research in both academic and industrial laboratories. Perhaps most notably, 5–10% of individuals with asthma experience severe asthma that is refractory to current medical treatment [1]. In addition, there are no therapies available to actively resolve the uncontrolled immune responses in asthma. Most individuals with asthma have airway inflammation that never completely resolves. The nature and extent of this inflammation varies by individual and by disease severity. In most cases, eosinophils and activated T cells accumulate in the lung. Th2 lymphocytes and eosinophils are increased in blood, lung tissue and bone marrow in most asthma clinical phenotypes. Many other cell types are implicated in the pathobiology of asthma and are likely to play prominent roles. Along these lines, many important functional responses have been assigned to mast cells, neutrophils and dendritic cells, as well as epithelial and mesenchymal cells [2]. These cells release inf lammatory mediators, including Th2-associated cytokines, chemokines, growth factors and lipid mediators that drive the inflammatory process. In some individuals, changes in the airway epithelium, basement membrane and smooth muscle remodel the airway, potentially leading to a component of fixed airflow obstruction.