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Human cutaneous leishmaniasis (CL) caused by  Leishmania braziliensis , presents an exaggerated Th1 response that is associated with ulcer development. Macrophages are the primary cells infected by  Leishmania  parasites and both reactive oxygen species (ROS) and nitric oxide (NO) are important in the control of  Leishmania  by these cells. The mechanism involved in the killing of  L .  braziliensis  is not well established. In this study, we evaluate the role of ROS and NO in the control of  L .  braziliensis  infection by monocytes from CL patients. After  in vitro  infection with  L .  braziliensis , the oxidative burst by monocytes from CL patients was higher when compared to monocytes from healthy subjects (HS). Inhibition of the ROS pathway caused a significant decrease in the oxidative burst in  L .  braziliensis  infected monocytes from both groups. In addition, we evaluated the intracellular expression of ROS and NO in  L .  braziliensis -infected monocytes. Monocytes from CL patients presented high expression of ROS after infection with  L .  braziliensis . The expression of NO was higher in monocytes from CL patients as compared to expression in monocytes from HS. A strong positive correlation between NO production and lesion size of CL patients was observed. The inhibition of ROS production in leishmania-infected monocytes from CL patients allowed the growth of viable promastigotes in culture supernatants. Thus, we demonstrate that while production of ROS is involved in  L .  braziliensis  killing, NO alone is not sufficient to control infection and may contribute to the tissue damage observed in human CL.

The Role of Nitric Oxide and Reactive Oxygen Species in the Killing of Leishmania braziliensis by Monocytes from Patients with Cutaneous Leishmaniasis