Abstract
Visceral leishmaniasis is associated with atrophy and histological disorganization of splenic compartments. In this paper, we compared organized and disorganized splenic lymphoid tissue from dogs naturally infected with Leishmania infantum assessing the size of the white pulp compartments, the distribution of T, B and S100+ dendritic cells, using immunohistochemistry and morphometry and the expression of CCR7 and the cytokines, CXCL13, lymphotoxin (LT)-α, LT-β, CCL19, CCL21, TNF-α, IL-10, IFN-γ and TGF-β, using by real time RT-PCR. The lymphoid follicles and marginal zones were smaller (3.2 and 1.9 times, respectively; Mann-Whitney, P<0.02) in animals with disorganized splenic tissue in comparison to those with organized splenic lymphoid tissue. In spleens with disorganized lymphoid tissue, the numbers of T cells and S100+ dendritic cells were decreased in the follicles, and the numbers of B cells were reduced in both the follicles and marginal zones. CXCL13 mRNA expression was lower in animals with disorganized lymphoid tissue (0.5±0.4) compared to those with organized lymphoid tissue (2.7±2.9, both relative to 18S expression, P = 0.01). These changes in the spleen were associated with higher frequency of severe disease (7/12) in the animals with disorganized than in animals with organized (2/13, Chi-square, P = 0.01) splenic lymphoid tissue. The data presented herein suggest that natural infection with Leishmania infantum is associated with the impairment of follicular dendritic cells, CXCL13 expression, B cell migration and germinal center formation and associates these changes with severe clinical forms of visceral leishmaniasis. Furthermore the fact that this work uses dogs naturally infected with Leishmania infantum emphasizes the relevance of the data presented herein for the knowledge on the canine and human visceral leishmaniasis.
Highlights
Visceral leishmaniasis is endemic in many parts of the world and is a significant health problem in Asia, Africa, Europe and the Americas
The sequential occurrence of hyperplasia followed by atrophy was demonstrated by Veress and collaborators [9] using an experimental model of visceral leishmaniasis in hamsters
We found that animals with active infection and cellular responses to Leishmania antigens, represented by positive leishmanin skin tests, predominantly displayed hyperplasia of the splenic white pulp, whereas atrophy and the disruption of splenic lymphoid architecture were more frequently seen in animals with active infection but negative leishmanin skin tests [10]
Summary
Visceral leishmaniasis is endemic in many parts of the world and is a significant health problem in Asia, Africa, Europe and the Americas. Visceral leishmaniasis exists in both anthroponotic and zoonotic forms that are caused by L. donovani and L. infantum, respectively [1]. The main clinical signs of visceral leishmaniasis include fever, hepatomegaly, splenomegaly, anemia, leukopenia, hypergamaglobulinemia and emaciation [2,3]. Death often results from cases of bleeding and from an increased susceptibility to secondary bacterial infection [3,4]. Dogs, which are one of the most common companion animals, are susceptible to visceral leishmaniasis, and canine visceral leishmaniasis shares many of the abovementioned aspects with the human disease. Dogs present with a more frequent and severe skin parasitism [6]. Evidence suggests that dogs are the main urban reservoir for L. infantum [7,8]
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