The eosinophil is the predominant inflammatory cell which accumulates in the asthmatic lung. There is considerable circumstantial evidence linking these cells to lung dysfunction, but the precise cause and effect relationship is controversial. The defensive role of the eosinophil appears to be concerned largely with eliminating helminth parasites which do not normally present a constant threat. Thus, unlike the neutrophil whose defensive role against microbes is essential, the eosinophil presents a target for therapeutic intervention which is potentially applicable to long-term treatment. Several approaches to suppressing eosinophil accumulation are possible, based on the multiple steps involved in their appearance and activation in the lung (for review see [1]). One approach is to block the receptor(s) to the important endogenous eosinophil chemoattractants generated in the asthmatic lung, offering the potential for selective leukocyte-type suppression. A first step in this pursuit is the identification of such chemoattractants. This article describes recent attempts in this direction, with the long-term goal of producing chemoattractant receptor antagonists.