Abstract
Canine Visceral Leishmaniasis (CVL) shares many aspects with the human disease and dogs are considered the main urban reservoir of L. infantum in zoonotic VL. Infected dogs develop progressive disease with a large clinical spectrum. A complex balance between the parasite and the genetic/immunological background of the host are decisive for infection evolution and clinical outcome. This study comprised 92 Leishmania infected mongrel dogs of various ages from Mato Grosso, Brazil. Spleen samples were collected for determining parasite load, humoral response, cytokine mRNA expression and histopathology alterations. By real-time PCR for the ssrRNA Leishmania gene, two groups were defined; a low (lowP, n = 46) and a high parasite load groups (highP, n = 42). When comparing these groups, results show variable individual humoral immune response with higher specific IgG production in infected animals but with a notable difference in CVL rapid test optical densities (DPP) between highP and lowP groups. Splenic architecture disruption was characterized by disorganization of white pulp, more evident in animals with high parasitism. All cytokine transcripts in spleen were less expressed in highP than lowP groups with a large heterogeneous variation in response. Individual correlation analysis between cytokine expression and parasite load revealed a negative correlation for both pro-inflammatory cytokines: IFNγ, IL-12, IL-6; and anti-inflammatory cytokines: IL-10 and TGFβ. TNF showed the best negative correlation (r2 = 0.231; p<0.001). Herein we describe impairment on mRNA cytokine expression in leishmania infected dogs with high parasite load associated with a structural modification in the splenic lymphoid micro-architecture. We also discuss the possible mechanism responsible for the uncontrolled parasite growth and clinical outcome.
Highlights
Canine Visceral Leishmaniasis (CVL) shares many aspects with the human disease and dogs are considered the main urban reservoir of L. infantum in zoonotic VL
The infection is characterized by a marked humoral response [10,11] and the parasite load follows the clinical outcome [12]
A relationship between a high percentage of T cell apoptosis and the structural disorganization of white pulp may co-contribute to the inefficient cellular-mediated-immune response in CVL [21]
Summary
Canine Visceral Leishmaniasis (CVL) shares many aspects with the human disease and dogs are considered the main urban reservoir of L. infantum in zoonotic VL. No conclusive data are available on the immunological mechanisms responsible for resistance or disease progression in CVL. In spleen the production of Th1 cytokines (such as IFN-γ, IL-12 and TNF) of both asymptomatic and symptomatic dogs does not show any differences [13,14,20], they are increased during infection [14]. The predominance of Th2/regulatory cytokines (such as IL-4, IL-10 and TGF-β1) determines the parasite load and persistence without association with clinical groups [14,15]. Correa et al [13] found that these cytokines are determinant for disease progression This organ is a site of parasite persistence where the parasites grow slowly generating important changes both in architecture and organ function. A relationship between a high percentage of T cell apoptosis and the structural disorganization of white pulp may co-contribute to the inefficient cellular-mediated-immune response in CVL [21]
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