Peripheral and tissue eosinophilia are associated with a wide variety
of inflammatory syndromes. These include both multisystem and limited
diseases with vasculitis or nonvasculitic tissue damage and variable e
xpression of end-stage-fibrosis. The idiopathic hypereosinophilic synd
rome (IHS) represents a multisystem disorder defined by sustained eosi
nophilia of an undetectable cause with significant organ system dysfun
ction. Although not specified as such in the criteria for the diagnosi
s of IHS, there are idiopathic eosinophilic syndromes that are clinica
lly distinct from IHS by virtue of the fact that the eosinophilic infl
ammation is limited to specific-tissues (such as the skin) with an ove
rall good prognosis. The pathogenic role of the eosinophilic granulocy
te in these conditions is attested by evidence of eosinophil activatio
n and degranulation at sites of tissue injury. The recruitment and loc
alization of eosinophils to specific sites of tissue inflammation invo
lves cytokines with haematopoetic growth factor activity, adhesion mol
ecules expressed both by the vascular endothelium and eosinophils,and
chemoattractants that stimulate eosinophil migration. Recently, overex
pression of IL-5 in transgenic mice was shown to lead to both peripher
al blood eosinophilia and tissue eosinophilia. With the advances in ou
r understanding of cytokine-dependent regulatory mechanisms that contr
ol the peripheral eosinophil number as well as the recruitment and sur
vivability of eosinophils at sites of inflammation, more targeted ways
of manipulating the eosinophil reaction can be expected in the future
.