Abstract
Inflammation is a major component in the pathology of chronic lung diseases, including asthma.
Anti-inflammatory treatment with corticosteroids is not effective in all patients. Thus, new therapeutic
options are required to control diverse cellular functions that are currently not optimally targeted by
these drugs in order to inhibit inflammation and its sequelae in lung disease. Peroxisome proliferator
activated receptors (PPARs), originally characterised as regulators of lipid and glucose metabolism,
offer marked potential in this respect. PPARs are expressed in both lung infiltrating and resident
immune and inflammatory cells, as well as in resident and structural cells in the lungs, and play
critical roles in the regulation of airway inflammation. In vitro, endogenous and synthetic ligands for
PPARs regulate expression and release of proinflammatory cytokines and chemoattractants,
and cell proliferation and survival. In murine models of allergen-induced inflammation, PPAR