Eosinophil trafficking to sites of allergic inflammation

Eosinophils play a prominent pro-inflammatory role in allergic inflammation . Studies utilizing flow chambers, intravital videomicroscopy, and cytokine and adhesion molecule-deficient mice have provided important insight into the mechanisms of eosinophil trafficking in inflamed blood vessels and into tissues in vivo. While the bone marrow generation of eosinophils is finely regulated by interleukin (IL)-5, the trafficking of eosinophils into tissu es is regulated by several cytokines, chemokines, and adhesion molecules wi th overlapping functions. Prospects for therapeutically inhibiting eosinoph ilic inflammation by inhibiting eosinophil adhesion to endothelium are depe ndent on an improved understanding of the relative importance of individual cytokines and adhesion molecules in regulating eosinophil adhesion to endo thelium. Alternative strategies to inhibit eosinophilic inflammation includ e the use of immunostimulatory DNA sequences containing a CpG motif to act as a Th1 adjuvant to prevent Th2 responses associated with IL-5 and eosinop hilia. Immunostimulatory DNA sequences do not induce eosinophil apoptosis, but function at the level of the bone marrow to inhibit the IL-5-induced bo ne marrow generation and release of eosinophils.