Serum nitrite level and adenosine deaminase activity is altered in visceral leishmaniasis

ABSTRACT In this study we sought to determine if there is alteration in nitric oxide (NO) production and adenosine deaminase (ADA) activity among patients with visceral leishmaniasis (VL) and the effect of four weeks of chemotherapy on these levels. Fifty-three VL patients diagnosed clinically and by direct demonstration of the LD bodies in the bone marrow smear were studied. They were treated with Sodium Stibogluconate and sampled at the baseline and four weeks. Forty-three healthy individuals coming from the same endemic area were taken as control. Total nitrite Keywords: NO, ADA, Visceral leishmaniasis INTRODUCTION Intramacrophage infection by Leishmania donovani (LD), an obligate intracellular protozoan, results the potentially fatal visceral leishmaniasis (VL) or kalaazar. The elimination of leishmania parasite by macrophage depends upon the mounting of effective cell-mediated immune response. During leishmaniasis infection, the microbicidal interaction between the parasite and host cells involves the presentation of leishmania antigen by macrophage to T-helper (Th) cell through MHC II molecule along with the co-stimulatory molecules (B7-1/B7-2 and CD40). 1, 2 Activation of Th cell causes proliferation of IFN-γ producing CD4+ Th subset. 3 IFN-γ and TNF-α, the defining cytokines of the Th1 subset in turn activates the macrophage to generate NO which is the most relevant anti-leishmanial oxidant. Contrary results have been found in the NO level during L. donovani infection both in vitro and in vivo experiments. 4, 5 Also studies reported hitherto have generally originated from in vitro culture and animal experiments. However no study has so far been conducted to investigate NO production in patients with visceral leishmaniasis. Therefore we aimed to determine serum nitrite level in VL patients as surrogate marker of NO production and compare it with the healthy subjects. Assessments of NO metabolites may be useful tool in the evaluation of the effector mechanism of macrophage and clinical manifestation of patients. Adenosine deaminase (ADA) is an essential for the proliferation, maturation and function of T lymphocytes. Its activity increases during antigenic and mitogenic responses of lymphocytes and is considered as an important immunoenzyme marker for assessing cell-mediated immunity in diseases characterized by T lymphocytes proliferation and maturation