[Idiopathic eosinophilia]

Peripheral and tissue eosinophilia are associated with a wide variety of inflammatory syndromes. These include both multisystem and limited diseases with vasculitis or non-vasculitic tissue damage and variable expression of end-stage-fibrosis. The idiopathic hypereosinophilic syndrome (IHS) represents a multisystem disorder defined by sustained eosinophilia of an undetectable cause with significant organ system dysfunction. Although not specified as such in the criteria for the diagnosis of IHS, there are idiopathic eosinophilic syndromes that are clinically distinct from IHS by virtue of the fact that the eosinophilic inflammation is limited to specific tissues (such as the skin) with an overall good prognosis. The pathogenic role of the eosinophilic granulocyte in these conditions is attested by evidence of eosinophil activation and degranulation at sites of tissue injury. The recruitment and localization of eosinophils to specific sites of tissue inflammation involves cytokines with haematopoietic growth factor activity, adhesion molecules expressed both by the vascular endothelium and eosinophils, and chemoattractants that stimulate eosinophil migration. Recently, overexpression of IL-5 in transgenic mice was shown to lead to both peripheral blood eosinophilia and tissue eosinophilia. With the advances in our understanding of cytokine-dependent regulatory mechanisms that control the peripheral eosinophil number as well as the recruitment and survivability of eosinophils at sites of inflammation, more targeted ways of manipulating the eosinophil reaction can be expected in the future.