Idiopathic eosinophilic pneumonia (IEP) is an uncom-mon disease of unknown aetiology characterized by theaccumulation of eosinophils in the lung, variable bloodeosinophilia and peripheral opacities on the chest radio-gram. The response to steroid treatment is dramatic butrelapses are frequent, requiring the use of long-termsteroid treatment [1].Eosinophils are primarily tissue cells, containing intheir granules many preformed proinflammatory andcytotoxic mediators [2]. They are also able to synthe-size many other substances that defend the host againstexogenous stimuli [3]; under normal conditions theeosinophil number in those tissues that have contact withthe environment is 200–400 times greater than in theblood [4]. An abnormally high accumulation of thesecells within the lung, frequency reaching up to 50% ofthe total alveolar cell population [5], is the hallmark ofIEP, but the role of the eosinophil in the immunopatho-genesis of lung damage in this disorder is still not com-pletely elucidated [4].Eosinophils accumulated within both interstitium andsmall air spaces [1] are hypodense and widely degran-ulated cells. They show typical morpho-functional char-acteristics of activated cells and are able to damageparenchymal lung structures by releasing a variety oftoxic substances [6]. Consequently, two major points needto be investigated and discussed: 1) how do eosinophilscause parenchymal injury? 2) how are eosinophils recruit-ed and activated at the site of inflammation?