Modulation of eosinophil chemotaxis

As in all biological systems, stimulating factors of eosinophil chemotaxis can be opposed by down-modulating factors. Such agents can inactivate eosinophilotactic factors, block their interaction with the cell and its receptor, or interfere with the complex cellular mechanism necessary for locomotion. Mediator antagonists such as antibodies to IL-5, IL-4 and MIP-la are very effective at inhibiting eosino phil accumulation in experimental models of allergic inflammation.

Among therapeutic drugs, corticosteroids and the immunosuppressant cyclosporine are well known, potent, rapidly acting reducers of blood and tissue eosinophil levels. Sympathomimetics and phosphodiesterase inhibitors have a similar effect. More recently, second-generation histamine H]-recepror antagonists (cetirizine, ketotifen) have been shown to have both in vivo and in vitro effects on eosinophil accumulation or migration. This effect is not shared by other E^-receptor antagonists. Also, leukotriene CysLT|-receptor antagonists and inhibitors of 5-lipoxygenase effectively suppress eosinophil recruitment in allergic inflammation.

In summary, many questions remain to be resolved in elucidating which factors govern the infiltration of eosinophils into tissue, their interplay with each other and with other factors, and their role in pathologic processes.

See also: Arachidonic acid and the leukotrienes; Chemotaxis; Eosinophils; Histamine; Interleukin 5 and its receptor; Mast cells; Platelet-activating factor (PAF).

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