The hypothesis that the diminished motility of human milk leukocytes is due to a decrease in adherence was tested by using a collagen gel system in which leukocyte movement is less dependent on adherence. Unfractionated human milk leukocytes (HML) or fractionated peripheral blood leukocytes were placed on collagen gels in microwells and the leading edge of migration was determined by inverted phase microscopy. The mean rates of invasion of HML, blood neutrophils, and mononuclear blood leukocytes were 14, 240, and less than 1 mu/h, respectively (p less than 0.01). We then examined the identity of motile HML by immunoperoxidase techniques using antibodies to selected cell markers. Motile HML were positive for a specific macrophage marker (cathepsin B) and a neutrophil and monocyte marker (Mac-1) but were negative for specific neutrophil (cathepsin G) or lymphocyte markers (CD3 and CD5). The directed motility of these cells was not enhanced by exposure to the chemoattractant, N-formyl-L-methionyl-L-phenylalanine, but was inhibited by a T cell lectin, phytohemagglutinin. The movement was actin dependent but was not dependent on calcium or Mac-1 surface glycoproteins. Thus, the diminished motility of milk neutrophils does not appear to be due to decreased adherence per se, and those HML that are motile are macrophages. This suggests a dichotomy for the function of HML. Neutrophils may be relegated to the lumen of th alimentary tract, whereas macrophages may penetrate into mucosal sites for host defense.

In a recent report we described a syndrome, identical to bowel-bypass syndrome, that occurred in four patients who had not had bypass surgery. Herein, circulating immune complexes (CICs) and neutrophil migration are evaluated in three of those four patients to test the hypothesis that the cutaneous lesions might have resulted from interaction between immune complex-mediated vessel damage and increased neutrophil migration. In vitro assays indicated that CICs were present in one of two patients and "histamine trap" test evidence for CICs was present in both patients tested. Although serum from the three patients appeared to increase neutrophil movement, statistically significant increases were not observed when data were pooled in this small study group. Preliminary results suggest that immune complex-mediated vessel damage, followed by extensive accumulation of neutrophils, may cause the pustular vasculitis in the bowel-associated dermatosis-arthritis syndrome.

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Oxidant-induced hemolysis, t h e hallmark of hexose monophosphate (HMP) shunt abnormalities, generally is not apprec i a t e d i n PK deficiency. I n v i t r o , however, some p a t i e n t s with PK deficiency manifest oxidant s e n s i t i v i t y (increased sulfhemoglobin formation) i n t h e presence of cyanide (CN) and ascorbate (Asc). The HMP shunt (glucose-l-14~ oxidation t o ' '~0~) of these PK d e f i c i e n t RBC's was stimulated by Asc t o t h e same extent a s were normal c e l l s . CN enhanced t h e Ascinduced HMF' stimulation i n control c e l l s , but inhibited t h e