Cytokine profile in Montenegro skin test of patients with localized cutaneous and mucocutaneous leishmaniasis

Abstract

SuMMarYAmerican tegumentary leishmaniasis presents as two major clinical forms: localized cutaneous leishmaniasis (LCL) and mucocutaneous leishmaniasis (MCL). The immune response in leishmaniasis is efficiently evaluated by the response to Leishmania antigen through the Montenegro skin test (MST). Both LCL and MCL present positive response to MST, indicating that the patients present cell-mediated immunity against the parasite -Leishmania. In spite of the presence of immunity in MCL, this is not sufficient to stop disease progression and prevent resistance to treatment. In this study we demonstrated interleukin (IL) 2, 4, 5 and interferon (IFN) gamma expression in biopsies of MST of ten patients with American tegumentary leishmaniasis. The obtained results were compared between LCL (n = 5) and MCL (n = 5) patients. The MST of MCL patients displayed a higher expression of IL-2, IL-4 and IL-5, in comparison to LCL. There was no significant difference in IFN-gamma expression between groups. The obtained results suggest the role of IL-4 and IL-5 in the maintenance of the immunopathogenic mechanism of the destructive lesions that characterize MCL.

Correlation of parasitic load with interleukin-4 response in patients with cutaneous leishmaniasis due toLeishmania tropica

“…The wide range of parasite burden observed in CL tissue lesions in the present study (200-10 6 parasites g À1 of dermal tissue) was comparable with the reported parasite load in CL lesions caused by various Leishmania spp. In human studies, MCL and intermediate ATL patients displayed a higher expression of IL-4 in comparison with LCL (Díaz et al, 2006;Nogueira et al, 2008). The study revealed unexpected findings in that the parasite load and IL-4 expression were higher in early lesions compared with late lesions, suggesting that the parasites might be multiplying rapidly during the onset of infection, inducing a Th2-type immune response.…”

“…The control of L. major lesion growth in genetically resistant mice has been clearly associated with the expansion of the T-helper type 1 (Th1) lymphocyte subset of the CD41 T-cell population and the production of the cytokines interferon-g (IFN-g) and interleukin-2 (IL-2) . In humans, American tegumentary leishmaniasis (ATL) showed a preponderance of IFN-g and IL-12 expression, whereas MCL patients displayed a higher expression of IL-2, IL-4 and IL-5, in comparison with localized cutaneous leishmaniasis (LCL) (Díaz et al, 2006;Nogueira et al, 2008). It has been shown that L. major and L. mexicana isolated from different clinical forms promote a different course of infection in BALB/c mice and the type of immune response elicited by the infected host (Satoskar et al, 1995;Kébaïer et al, 2001).…”

“…It has been shown that L. major and L. mexicana isolated from different clinical forms promote a different course of infection in BALB/c mice and the type of immune response elicited by the infected host (Satoskar et al, 1995;Kébaïer et al, 2001). In humans, American tegumentary leishmaniasis (ATL) showed a preponderance of IFN-g and IL-12 expression, whereas MCL patients displayed a higher expression of IL-2, IL-4 and IL-5, in comparison with localized cutaneous leishmaniasis (LCL) (Díaz et al, 2006;Nogueira et al, 2008).…”

Montenegro Skin Test and Age of Skin Lesion as Predictors of Treatment Failure in Cutaneous Leishmaniasis

“…MST is a marker of cellular immune response 10 , evaluating type IV hypersensitivity response mediated by T cells 28 . However, it may be influenced by clinical presentation 18 and by disease duration 7,15 .…”

Mechanisms of Immunopathology of Leishmaniasis

“…MCL, on the other hand, is associated with mixed Th1 and Th2 immune responses (Castes and Tapia 1998 ). Higher IL-2, IL-4, and IL-5 production has been observed in MCL causing L. braziliensis compared to LCL causing L. braziliensis (Nogueira et al 2008 ). Tissue destruction in MCL has been attributed to higher concentrations of TNF-α and the cytolytic action of CD8 + T cells, NK cells, and neutrophils (Nylen and Eidsmo 2012 ;Blackwell 1999 ).…”