FAGOCITOSIS EN LEPRA

The function of phagocytic cells is of great importance for the control of most infectious diseases. In leprosy, this is particularly important as M. leprae not only parasitizes these cells but uses them to survive. It has been reported that macrophages from lepromatous patients are less efficient than their normal counterparts in their ability to digest M. leprae. This deficiency, however, has been better explained on the basis of a defective cell mediated immunity at the level of T-lymphocytes reactive to M. leprae antigens. Polymorphonuclear phagocytes (PMNs) of lepromatous patients, on the other hand, do not seem to be defective in their metabolic functions when compared to PMNs from healthy subjects. These cells show normal (or slightly increased) levels of the different hydrolytic enzymes so far studied (acid and alkaline phosphatases, lipase, β-galactosidase, β-glucuronidase, myeloperoxidase, RNase, DNase, and some others). They also show the phagocytosis-induced metabolic changes that characterize normal PMNs. Nevertheless, an important proportion of patients shows a depressed endocytic ability (roughly 40% in relation to controls). Most probably, and based on the above data, this endocytic defect is not the result of a defect in the phagocytes themselves, but of the action of soluble factors present in the blood of lepromatous patients as lepromatous serum causes a comparable depression in the endocytic function of circulating phagocytes. The nature of these factors can be multiple but circulating immune complexes could be involved as they are present in many lepromatous patients. These results receive support from others in the literature that indicate the existence in lepromatous serum of soluble factors able to block the chemotactic response of phagocytes both in vivo and in vitro, and from others from our laboratory that indicate a depressed ability of lepromatous phagocytes to adhere to plastic surfaces. These abnormalities in the phagocytic function might explain, at least in part, the defective inflammatory responses observed in lepromatous patients to several inflammatory stimuli.