Using Boyden chambers, Prostaglandin A1 (PGA1) was shown to inhibit directed movement of polymorphonuclear (PMN) leucocytes to the chemoattractants endotoxin-activated serum and casein, and in random migration systems. Depressed chemotaxis could not be entirely attributed to defective random migration, as the drug was shown to inhibit both chemokinesis (stimulated random migration) and "true chemotaxis". In addition, PGA1 inhibited the movement of neutrophils out of capillary tubes and substantially reduced hexose monophosphate shunt (HMPS) activity. Mice injected with PGA1 demonstrated significantly less PMN movement into trypticase-soy-broth-induced peritoneal exudates, and it is postulated that during inflammatory processes release of PGA1 increases cell accumulation at the site, thereby amplifying the inflammatory response.