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Eosinophil trafficking to sites of allergic inflammation
Author(s) -
Broide David,
Sriramarao P.
Publication year - 2001
Publication title -
immunological reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.839
H-Index - 223
eISSN - 1600-065X
pISSN - 0105-2896
DOI - 10.1034/j.1600-065x.2001.790116.x
Subject(s) - eosinophil , inflammation , allergic inflammation , eosinophilia , chemokine , immunology , cytokine , cell adhesion molecule , biology , eosinophil cationic protein , intravital microscopy , bone marrow , interleukin 5 , major basic protein , microbiology and biotechnology , in vivo , interleukin , asthma
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 tissues is regulated by several cytokines, chemokines, and adhesion molecules with overlapping functions. Prospects for therapeutically inhibiting eosinophilic inflammation by inhibiting eosinophil adhesion to endothelium are dependent on an improved understanding of the relative importance of individual cytokines and adhesion molecules in regulating eosinophil adhesion to endothelium. Alternative strategies to inhibit eosinophilic inflammation include 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 eosinophilia. Immunostimulatory DNA sequences do not induce eosinophil apoptosis, but function at the level of the bone marrow to inhibit the IL‐5‐induced bone marrow generation and release of eosinophils. This research was supported by NIH grants AI 38425 and AI 33977 (DHB) and AI 35796 to (PS).