Phagocytosis in leprosy. 5. The effect of the infection with Mycobacterium lepraemurium on the level of diverse hydrolytic lysosomal enzymes of murine peritoneal macrophages.

The effect of the infection with M. lepraemurium on the activity of several lysosomal enzymes of mouse peritoneal cells was studied. The enzymes studies were acid- and alkaline-phosphatases, acid (cathepsin D-type) proteinase, beta-glucuronidase, deoxyribonuclease, a nonspecific lipase, and lysozyme. Enzyme determinations were carried out four months and six months after the infection with 15.5 X 10(7) bacilli per mouse. Clear differences between M. lepraemurium-infected and normal animals were observed at four months of infection, with all of the mentioned enzyme activities well above the normal values. At six months of infection, a tendency to decrease to normal values of the enzyme activities was observed. It is suggested that this biochemical activation of mouse peritoneal cells reflects the effect of the cell-mediated immune response triggered by the infection with the murine leprosy bacillus. M. lepraemurium-infected mice possess macrophages in a high state of biochemical activation; yet, they are unable to get rid of the infecting microorganism.

Phagocytosis in leprosy. III. Defective adhesive and endocytic abilities of circulating leukocytes in lepromatous leprosy.

Two aspects of the phagocytic process in normal and lepromatous polymorphonuclears (PMN) and monocytes (MN) were studied. These aspects were endocytosis and adherence to surfaces. These 2 phenomena are closely related to each other and to the whole phagocytic process as they depend on membrane activity. It was found that both lepromatous phagocytes (PMN and MN) show, on the average, a depressed ability to endocytose opsonized Mycobacterium lepraemurium when compared to normal phagocytes. This impairment, however, does not seem to be related to intrinsic defects in the phagocytic cells themselves but to the presence in lepromatous serum of factors that interfere with the endocytic function. This conclusion was drawn from the fact that lepromatous serum causes a similar diminution in the endocytic ability of normal phagocytes. On the other hand, lepromatous plasma but not indeterminate leprosy nor normal plasmas interfere with the capacity of PMN leukocytes to adhere in vitro to plastic surfaces. These impairments in the phagocytic function might help to better understand the depressed overall inflammatory responses observed in vivo in lepromatous patients with a long-lasting disease.