Leprosy is an infectious diseases caused by Mycobacterium leprae. It is considered to be manifested in person with an impaired. immune system and is divided into two polar forms; the first being tuberculoid leprosy(TL) with nearly norrnal cell-mediated immunity(CMI) and the second heing lepromatous leprosy(LL) with deficient CMI. Adenosine deaminase(ADA) is an enzyme concerned with intermediary purine metabolism, which is known to be deficient in case of immunological dysfunction. To find out if there is any ADA deficiency in leprosy, the ADA activities in the lymphocytes of leprosy patients were compared with those of normal ones. The ADA activities in lymphocytes of normal subjects, TL patients and. LL patients were as follows; ID. 36-I-l. 90 units/10cells, 6. 35+0. 86units/10'cells and 4. 58+0. 52units/IO'cells respectively. The ADA activities in lymphocytes were revealed to be significantly different between normal subjects and LL patients(p<0. 01) and also between normal subjects and TL patients(p<0. 05). The lowered ADA activities in lymphocytes of leprosy patients, particularly in lepromatous leprosy, suggests a similar role in ADA for immunological response as demonstrated in severe combined immunodeficiency diseases.
Adenosine Deaminase* ; Adenosine* ; Communicable Diseases ; Humans ; Immune System ; Leprosy* ; Leprosy, Lepromatous ; Lymphocytes* ; Metabolism ; Mycobacterium leprae ; Severe Combined Immunodeficiency

The cause responsible for the lack of an efficient cell-mediated immunity or a delayed type hypersensitivity to M. leprae in lepromatous patients is poorly understood. But the resistance to M. leprae infection in humans is likely mediated by the activated macrophages to present M. leprae antigen to T cells for cell-mediated immunity. Phenolic glycolipid-I (PGL-I) is a M. leprae-specific antigen and is supposed to play a significant role in the long lasting unresponsiveness in lepromatous leprosy. In this study, IL-1 activities were tested among leprosy patients to evaluate monocyte function and the role of IL-1 in the immunosuppression in leprosy. We found that peripheral blood mononuclear cells (PBMCs) from tuberculoid patients were strongly reactive to M. leprae (mean cpm; 28,853 +/- 28,916), but the proliferative responses of PBMCs from lepromatous patients (mean cpm; 6,051 +/- 803) were significantly lower. IL-1 concentration in culture supernatant of monocytes from lepromatous patients was similar to that from tuberculoid patients with stimulation of M. leprae (lepromatous: 1,014 +/- 637 pg/ml, tuberculoid: 1,012 +/- 167 pg/ml) or lipopolysaccharides (IPS) (lepromatous: 3,479 +/- 2,188 pg/ml, tuberculoid: 4,246 +/- 2,432 pg/ml). The IL-1 concentration is sera from lepromatous patients (42 +/- 30 pg/ml) tended to be higher than those from tuberculoid patients (28 +/- 69 pg/ml). And there was no significant difference in IL-1 production between peritoneal macrophages from mice sensitized with PGL-1 and those from nonsensitized mice. In conclusion, this study suggests that the immunosuppression in lepromatous patients may not be due to the decreased production of IL-1. And the increased IL-1 activity in sera may affect the inflammatory response of lepromatous patients.
Glycolipids/pharmacology ; Human ; Immunity, Cellular ; Interleukin-1/*biosynthesis ; Leprosy, Lepromatous/blood/*metabolism ; Lymphocyte Activation ; Monocytes/*metabolism ; Mycobacterium leprae/metabolism ; Support, Non-U.S. Gov't

Adult ; Female ; Heat-Shock Proteins ; genetics ; Humans ; Leprosy ; diagnosis ; genetics ; microbiology ; Male ; Middle Aged ; Mycobacterium leprae ; pathogenicity ; Polymerase Chain Reaction ; methods ; Polymorphism, Restriction Fragment Length ; Skin ; metabolism