Abstract
The eosinophil was first named by the brilliant German scientist Paul Ehrlich in 1879, while he was experimenting with aniline dyes to stain blood cells and tissues. He also discovered neutrophils, basophils, and mast cells. The highly basic proteins in cytosolic granules of a small subpopulation of cells in human blood stained vivid pink with the acid dye eosin (from the Greek “eos” meaning dawn), hence “eosinophils.” He subsequently observed high numbers of these cells in the sputum of asthmatic patients and recognized the close relationship between eosinophilia and the severity of asthma. Pertinent to our story was his proposition that a “material which attracts eosinophils” exists. Further, he postulated that eosinophils and neutrophils possess different “chemotactic irritability” and that eosinophils only migrate to sites where a “specific stimulating substance” is present (1).
Highlights
This could have been the inspiration behind the Eotaxin project but, in truth, its origins were more prosaic
We seemed to be on another planet; clearly, the world of asthma was orbiting around the eosinophil
The plan to combine the two techniques as an in vivo generating and in vivo bioassay system to identify endogenous eosinophil chemoattractants was submitted to the asthma charity as a project grant, but sadly this was rejected with not unreasonable reservations about feasibility
Summary
This could have been the inspiration behind the Eotaxin project but, in truth, its origins were more prosaic. To provide a brief background, my Ph.D. project on mechanisms of inflammation involved the measurement of microvascular plasma protein leakage in rabbit and guinea pig skin using 125I-albumin as a marker. We began experiments with 111In-neutrophil trafficking in vivo, and the purification and identification of C5a brought us into contact with an expert protein sequencing group in London.
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