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The function of polymorphonuclear leucocytes (PMNs) was examined in 33 workers with occupational exposure to organochloride insecticides. A deep impairment of chemotaxis, adhesion, phagocytosis and nitroblue tetrazolium-dye reduction was found. A simultaneous increase of random migration and stimulated migration was observed. Perhaps the increase of the surface migration of leucocytes can partially compensate for the decrease of chemotaxis. However, no correlation between chemotaxis and spontaneous or stimulated migration could be demonstrated. The failure of PMN incubation in autologous serum to affect leucocyte migration and the fact that chemo-attractant generated from the plasma of both workers and controls show similar activity both suggest that the damaged PMN chemotaxis is not serum but cell-dependent. The simultaneous increase of infectious disease, especially of the upper respiratory tract, was found in the group of workers chronically exposed to organochloride insecticides. This kind of infection in the examined group of workers depends mainly on the chronic exposure to insecticides and only partially on the observed impairment of leucocyte function. A possible cause for the frequency of infections in workers is discussed.

Chemotaxis and random migration of neutrophils under agarose were compared between untreated ulcerative colitis patients (35 women and 36 men) and healthy subjects (25 women and 28 men). The ulcerative colitis patients were divided into two subgroups--those with the active (no. = 41) and those with the inactive (no. = 30) stage of the disease. High spontaneous mobility and subnormal chemotaxis (both aberrations statistically significant) were noted in the ulcerative colitis patients. Polymorphonuclear leukocyte chemotaxis was significantly lower in inactive than in active colitis. Possible causes of the difference in neutrophil chemotaxis between the two disease groups were discussed. No difference in the chemotactic activity between zymosan-stimulated plasma from controls and patients was found. The defect in the chemotaxis of neutrophils in ulcerative colitis might explain the small abscesses persisting in the mucosa of the great bowel.

The chemotactic migration in vitro of intestinal macrophages and peripheral blood monocytes has been assessed in patients with Crohn's disease, ulcerative colitis, and miscellaneous intestinal diseases. In all groups, the chemotaxis of peripheral blood monocytes was similar to that of healthy subjects. Intestinal macrophages migrated similarly to autologous monocytes in patients with ulcerative colitis and in the miscellaneous group. In contrast, intestinal macrophages from patients with Crohn's disease exhibited a wide range of chemotaxis from markedly suppressed to normal. This variation was independent of drug treatment and the degree of inflammation present. However, patients in whom granulomata were not present exhibited a significant depression of chemotaxis compared with those with granulomata, with disease controls (ulcerative colitis patients), and with the miscellaneous group. Such a difference was not reflected in monocytes from autologous peripheral blood. These findings indicate the presence of local mucosal suppressive factors in some patients with Crohn's disease and could suggest that the diminished ability of macrophages to accumulate in a focus of inflammation may be an underlying mechanism for the failure to form granulomata in these patients.