The emigration sequence and cytology of acute inflammation produced by a variety of stimulants was studied in dogs using a modified skin window procedure. Control lesions revealed the typical acute inflammatory cycle with an early influx of polymorphonuclear neutrophils and a later increase in lymphocytes, hypertrophied lymphocytes and macrophages.

Either fibrinogen, fibrin or proteolytic enzymes that promote fibrin formation selectively attracted eosinophils into the inflammatory site. Neither histamine nor albumin produced significant eosinophil migration in the 10 hours under study.

The fluorescent antibody technic was employed to assess the level of cellular profibrinolysin. Only inflammatory eosinophils and bone marrow eosinophils were marked with rhodamine antiprofibrinolysin. Staining was confined to intra- and extracellular eosinophil granules and coalesced masses. The intensity of fluorescence varied somewhat and perhaps reflected profibrinolysin release into the inflammatory exudate.

Exudative eosinophils like all members of the bone marrow eosinophilic series contain profibrinolysin localized in the specific granules. Eosinophils which migrate and collect at an inflammatory site clearly transport profibrinolysin to an area of fibrin deposition. Granule release of profibrinolysin provides one mechanism for fibrinolysis that likely facilitates wound repair.

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