The precise details by which circulating blood cells interact with the vascular surface and eventually emigrate from the blood have long held the interest of animal physiologists. The earliest descriptions of this response to inflammatory stimuli date to 150 years ago, and were the subject of an extensive series of lectures in 1889 by Cohnheim (1). Cohnheim with remarkable foresight predicated that" that it is solely the vessel wall which is responsible for the entire series of [inflammatory] events". Moreover his experiments led him to the remarkably precient conclusion that" inflammation is the expression and consequence of a molecular alteration in the vessel walls." This remarkable conclusion

-considering that Kebul6 had only imagined how carbon atoms could form molecules in 1854-was sparked by the observation that focal injurious or inflammatory stimuli results in the accumulation of what we now know to be leukocytes only at the point of application of the stimuli. The side of the microvasculature away from, or downstream of, the stimulus remained free of leukocytes. The tightly focused nature of the response suggested that only a structure fixed in space, as opposed to a primary effect on the circulating cells as proposed in Virchow's cellular theory of inflammation, could account for this rapid and specific change. Cohnheim understood that the blood being in continual motion could not account for the initial response that generated spatial locali-zation of leukocyte adhesion and extravasation. The rapid progress in the field of inflammation over the last dozen years has revealed the nature of the molecules anticipated by Cohnheim. We now understand much of the molecular basis for what we here will call immediate inflam-matory responses, and those with a delayed onset where the response takes more than an hour to become evident (2, 3). Although the molecules involved differ between these processes, the general principle of immediate and delayed responses are quite similar. In both cases, endothelial cells are stimulated to express members of the selectin family of adhesion proteins that bind constitutively expressed counterreceptors on passing leukocytes (4). This interaction accounts for leukocyte rolling along the vascular endothe-lium, rather than the light adhesion that is responsible for