Intracellular pathogenic protozoan infection like visceral leishmaniasis is considered in terms of the overall inflammatory response and the complex cellular interactions leading to formation of the activated macrophage. Analysis of the development of activation is facilitated when operationally defined stage of activation are characterized using a library of objective markers. There is a role of arginase in the immune response supporting its involvement in macrophage effector mechanism in vitro and in vivo. 5′-Nucleotidase a plasma membrane component has been cited as a biochemical correlate of macrophage function in an altered morphological and biochemical state of activation and stimulation. Depression in 5′-nucleotidase activity has been generally referred to as a characteristic marker of activated macrophages. Lysozyme or lysosomal enzymes are released into the endocytic or autophagic vacuole macrophage where they serve the purpose of intracellular digestion of engulfed or segregated materials. In the present study, we have studied levels of arginase and 5′-nucleotidase (marker for macrophage activation) in monocytes of active VL patients and healthy controls. Lysozyme a secretary product of macrophages was also measured in supernatants collected from monocytes of active VL patients and healthy controls. Elevated levels of 5′-nucleotidase were observed in supernatants of monocytes from active VL patients as compared to healthy controls. Low levels of arginase and lysozyme production by monocytes isolated from VL patients were observed as compared to healthy controls. Our studies suggest that low levels of arginase and elevated 5′-nucleotidase activity could be one of the mechanisms in the pathology of VL infection. Low lysozyme activity in patients may account for persistence of Leishmania parasites in VL infections.

BACKGROUND:Serum adenosine deaminase (ADA) activity increases in diseases where cellular immunity is involved. Since cell-mediated immune responses play a paramount role in the pathogenesis and healing of the visceral leishmaniasis, therefore, the present study was undertaken to evaluate the serum ADA activity in different pathological conditions. METHODS:Adenosine deaminase was determined in sera of active visceral leishmaniasis (VL) patients at diagnosis and at posttreatment (n=22), healthy controls (n=15), patients with malaria (n=10), leprosy (n=10) and tuberculosis (n=10). RESULTS:Serum levels of ADA were significantly higher in active VL patients as compared to controls and patients with other diseases. ADA levels were also raised in patients with malaria, though not significantly as compared with active VL patients. Sera from VL patients at posttreatment showed significantly decreased ADA levels over sera from patients at diagnosis. CONCLUSIONS:The results therefore suggest that ADA is involved in the pathogenesis and could be used as a clinical marker in the diagnosis of visceral leishmaniasis.