Abstract
BackgroundCanine leishmaniosis (CanL) due to Leishmania infantum is characterized by the development of both cellular and humoral immune responses. The dysfunction of T cell-mediated immunity leads to a lack of proliferation of T cells in response to Leishmania antigens with the consequence of parasite dissemination that seems to be related to a T cell exhaustion mediated by regulatory B cells expressing immunoglobulin D (IgD). The aim of this study was to determine and compare the total serum IgD in dogs with clinical leishmaniosis and in clinically healthy dogs.ResultsA total of 147 dog sera were studied. All dogs were tested for L. infantum-specific antibodies by quantitative ELISA. Interferon-gamma (IFN-γ) production was also determined by sandwich ELISA after blood stimulation with L. infantum soluble antigen (LSA) or concanavalin A (ConA). The quantification of total IgD was performed using a human IgD sandwich ELISA quantification set. Dogs were classified in three different groups. Group 1 included 40 clinically healthy non-infected dogs, all serologically negative to L. infantum-specific antibodies and non-producers of IFN-γ upon LSA stimulation. Group 2 included 63 clinically healthy infected dogs that were LSA IFN-γ producers (n = 61) and/or IFN-γ non-producers (n = 2) as well as negative to medium seropositive to L. infantum antigen. Finally, Group 3 included 44 dogs with clinical leishmaniosis (IFN-γ producers, n = 23; and IFN-γ non-producers, n = 21) that were negative to highly positive to L. infantum-specific antibodies. No significant differences were observed when the total IgD concentration was compared within groups. Additionally, total IgD of sick IFN-γ producers and IFN-γ non-producers was not significantly different. Finally, total IgD concentration was not statistically related to demographic parameters such as age, sex and breed.ConclusionsThe results of this study demonstrated that there were no differences between groups in total serum IgD. Total serum IgD does not appear to be a marker of disease in CanL.
Highlights
Canine leishmaniosis (CanL) due to Leishmania infantum is characterized by the development of both cellular and humoral immune responses
Control healthy non-infected dogs were all IFN-γ non-producers with lower production after L. infantum soluble antigen (LSA) (MannWhitney U-test: Z = -8.31, P < 0.0001) and concanavalin A (ConA) (MannWhitney U-test: Z = -2.67, P = 0.008) stimulation when compared with control healthy infected IFN-γ producers (Fig. 1a, b)
This study demonstrates that there is no clear increase of total serum immunoglobulin D (IgD) in dogs with clinical leishmaniosis when compared with healthy dogs, a trend was found
Summary
Canine leishmaniosis (CanL) due to Leishmania infantum is characterized by the development of both cellular and humoral immune responses. Canine leishmaniosis (CanL) is a vector-borne disease caused by the protozoan Leishmania infantum, which is mainly transmitted from dog to dog by female sand flies of the genus Phlebotomus in Europe [1] and Lutzomyia spp. in the New World [2]. Leishmania infantum infection does not always indicate the development of a clinical disease [5]. This infection can manifest as a chronic subclinical infection, self-limited disease or a severe fatal disease. Dogs with mild to moderate clinical stages present higher interferon-gamma (IFN-γ) production, low parasite load and antibody response when compared to the more severe stages [8, 9]
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