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Experimental diabetes was induced in rats by the injection of str eptozotocin. Peritoneal polymorphonuclear leucocytes (PMNLs) and macrophages were induced by i .p. injection to diabetic and normal rats with glycogen and chemotaxis assay was performed in multi-well chemotaxis chamber s with polycarbonate membrane filters. Sera of diabetic and normal rats were activated as a chemoattractant with E. coli lipopolysaccharide. Although both PMNLs of diabetic and normal rats migrated to activat ed serum obtained from a normal rat, significantly lower levels of chemotactic responses were detected in PMNL s of diabetic rats. I n the kinetics of serum elaboration of PMNL chemotactic activity , migration of PMNLs from normal rats continued to increase throughout the 60 min incubation period a nd reduced in next 30 min. However, PMNLs of diabetic rats migrated similarly within the first 45 min and de creased from 60 to 90 min after stimulation. And same results were obtained in the experime nts with serum from a diabet-i c rat as the chemoattractant. In case of the kinetic experiment of macrophage chemotactic activity el aborated by serum, no significant difference was detected in the macrophage migration from normal rats and diabetic rats within 90 min after stimulation. Although, from 90 to 105 mins , migration of macrophages obtained from normal rats remained relatively constant , continuous and significant increase was observed in macrophages from diabetic rats. When the serum from a diabetic rat was used as the chemoattractant, the same results were obtained. In conclusion, the leucocyte chemotactic responses were abnormal in diabetic r ats, and this abnormal f unction was not induced by diabetic serum. Thus, it seems that the abnormality of the leucocyt e che-motaxis may play a role i n the decreased resistance to infections in diabetes .

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