Polymorphonuclear leucocyte function was investigated in 19 patients with active Behçet's disease. Spontaneous free leucocyte migration was found to be significantly reduced, yet after stimulation the leucocyte's chemotactic activity was considerably increase (p less than 0-05) when compared to control leucocytes. Control leucocytes migrated more rapidly when incubated in serum taken from patients with Behçet's disease (p less than 0-005). The enhanced chemotactic activity in Bechçet's disease appears to be due to both serum and intrinsic leucocyte factors. Spontaneous nitroblue tetrazolium reduction was found to be normal, although after stimulation leucocyte nitroblue tetrazolium reduction was lower than in the control group (P less than 0-025), as was leucocyte oxygen utilisation. It is suggested that the hyperreactive cellular inflammatory response that characterises Behçet's disease may be due to increased chemotactic activity and minor alterations in functional metabolic activity of leucocytes.

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In quantitative experiments using ELISA, binding of Tamm-Horsfall protein (THP) to uropathogenic Escherichia coli was studied with monoclonal antibody to THP. Adherence to E. coli bearing type 1 fimbriae was proportional to THP concentration and size of the bacterial inoculum. Type 1 fimbriae-bearing E. coli bound 50 times more THP than did non-type 1-fimbriated or P-fimbriated strains. Concanavalin A and wheat germ agglutinin bound THP in a dose-dependent fashion, whereas pokeweed mitogen and Vicia villosa B4 isolectin did not. Addition of mannose and N-acetylglucosamine reduced adherence of THP to concanavalin A and wheat germ agglutinin by 50%-80%. Sugar inhibition studies suggested that the fimbrial receptor site for THP has lectin-like properties and that THP binds to fimbriae via its mannose side chains. This quantitative assay is useful for studying the interaction between THP, uroepithelial cells, and bacteria in vitro.

The in vitro adherence of multiple 14C-glucose labeled isolates of Candida albicans to exfoliated vaginal epithelial cells in the presence of subinhibitory concentrations of ketoconazole was studied with a new method utilizing differential centrifugation in a gelatin-PBS solution as well as by the standard method of direct microscopy measurement. Pre-incubation of stationary-phase candida in ketoconazole at concentrations of 0.002 to 0.1 microgram/ml for 4 h at 37 degrees C had no effect on adherence. The addition of ketoconazole to logarithmic phase Candida albicans failed to reduce the total number of cell-associated adherent yeast but exposure to subinhibitory concentrations of ketoconazole was associated with a dystrophic morphology of the blastospores, extensive clumping and reduced germination resulting in fewer individual candida blastospores directly attached to the cell membranes. Germination inhibition and a marked reduction in adherent candida was observed when 0.01 microgram/ml ketoconazole was added to Candida albicans incubated in germination promoting medium. The diminished adherence of Candida albicans to vaginal epithelial cells after exposure to subinhibitory concentrations of ketoconazole may have clinical relevance in preventing recurrent candida vaginitis.

Since MS-fimbriated bacteria adhere to Tamm-Horsfall protein, it has been suggested that Tamm-Horsfall protein may trap urinary pathogens and prevent them from colonizing the mucosal surfaces of the urinary tract. To test the hypothesis that low urinary Tamm-Horsfall protein excretion rates predispose to urinary tract infection we obtained serial urine samples from 17 women with and 18 without a history of recurrent urinary tract infection. None of the women had known structural abnormalities of the urinary tract. Concentrations of Tamm-Horsfall protein in urine were measured with a sensitive enzyme-linked immunosorbent assay method. On the average, 3 urine samples per person collected within 3 to 6 months were analyzed. The mean Tamm-Horsfall protein excretion of women with recurrent urinary tract infection was 57.0 mg./l. and that of controls was 66.3 mg./l.; this difference was not statistically significant. The mean coefficient of variation was 44.2 and 62.1%, respectively. We conclude that urinary Tamm-Horsfall protein concentration is not significantly decreased in women with recurrent urinary tract infection compared with controls, and that excretion varies widely in repeat samples obtained from the same individual.