Immune Response in Human Visceral Leishmaniasis: Analysis of the Correlation Between Innate Immunity Cytokine Profile and Disease Outcome

Abstract

We investigated the cytokine profile of cells of the innate immune response and its association with active

Cytokines and visceral leishmaniasis: a comparison of plasma cytokine profiles between the clinical forms of visceral leishmaniasis

“…The plasma concentrations of most of the analysed cytokines (IFN-γ, TNF-α, IL-4 and IL-10) were higher in the subjects with active VL relative to the other groups, demonstrating an exacerbation of the immune response in these patients; this elevation in cytokine levels is in agreement with results from other studies (Hailu et al 2004, Peruhype-Magalhães et al 2005, Kurkjian et al 2006, Khoshdel et al 2009). Here, a mixed cytokine profile (Th1 and Th2) was detected in the patients with the active disease.…”

“…Here, a mixed cytokine profile (Th1 and Th2) was detected in the patients with the active disease. This mixed profile has also been reported by other investigators (Goto & Lindoso 2004, Peruhype-Magalhães et al 2005, Goto & Prianti 2009). The increase in inflammatory cytokines could be associated with the physiopathological alterations seen during the active disease, whereas the production of IL-10 has been suggested to be important for the survival and persistence of the parasite inside macrophages (PeruhypeMagalhães et al 2006.…”

“…In experimental mouse models using Leishmania major, protection against the disease is attributed to a T helper (Th)1 immune response that is characterised by the production of interferon (IFN)-γ and interleukin (IL)-12, whereas susceptibility to the disease is attributed to a Th2 type response with the production of IL-4 and IL-10 (Park et al 2000, Belkaid et al 2002, Stetson et al 2002, Goto & Prianti 2009). However, this dichotomy is not evident in mice infected with Leishmania donovani (Melby et al 2001, Peruhype-Magalhães et al 2005. In humans, VL is considered to be the prototype of immune dysfunction, compromising both cellular and humoral immunity.…”

“…These clinical forms reflect the balance between the multiplication of the parasite in mononuclear phagocytes, the host immune response and the degenerative conditions resulting from the infection (Medeiros et al 1998, Peruhype-Magalhães et al 2005, MS/SVS 2009). The factors that determine the development of VL have not been completely identified, but the specific cellular immune response to Leishmania seems to play a key role in the control of infection (Holaday 2000, Bacelar & Carvalho 2005, Michalick & Genaro 2005.…”

“…The immunological mechanism involved in the infection and the relationship between the immune system and the clinical forms of the disease have been studied by evaluating cellular profiles and cytokine production in bone marrow, spleen and lymph node aspirates, as well as in peripheral blood mononuclear cells and in plasma samples from patients with different clinical forms of VL. Analysis of plasma samples is a suitable alternative to the other methods because it is simpler and less invasive (Hailu et al 2004, Peruhype-Magalhães et al 2005, Khoshdel et al 2009). …”