Abstract
Parasite co-evolution alongside the mammalian immune system gave rise to several modulatory strategies by which they prevent exaggerated pathology and facilitate a longer worm survival. As little is known about the immunoregulatory potential of the zoonotic canine parasites Ancylostoma caninum and Toxocara canis in the natural host, the present study aimed to investigate whether their larval excretory-secretory (ES) products can modulate the canine immune system. We demonstrated TcES to increase the frequency of CD4+ Foxp3high T cells, while both AcES and TcES were associated with elevated Helios expression in Foxp3high lymphocytes. ES products were further capable of inducing IL-10 production by lymphocytes, which was mainly attributed to CD8+ T cells. ES treatment of PBMCs prior to mitogen stimulation inhibited polyclonal proliferation of CD4+ and CD8+ T cells. Moreover, monocyte-derived ES-pulsed dendritic cells reduced upregulation of MHC-II and CD80 in response to lipopolysaccharide. The data showed that regulation of the canine immune system by A. caninum and T. canis larvae comprises the modification of antigen-specific and polyclonal T cell responses and dendritic cell maturation.
Highlights
Parasites are responsible for public health problems worldwide with the highest prevalence being attributed to intestinal helminths[1,2,3]
To evaluate whether A. caninum and T. canis larvae share a Treg inducing ability, canine peripheral blood mononuclear cells (PBMCs) were cultured in the presence of AcES and T. canis ES (TcES) for 72 hours and analysed with respect to their Foxp[3] expression by flow cytometry
Co-staining for CD4 and CD8 revealed the TcES-associated increase in Foxp3high expression to be associated with CD4+, CD4 + CD8+ and CD4- CD8- double-negative T cells
Summary
Parasites are responsible for public health problems worldwide with the highest prevalence being attributed to intestinal helminths[1,2,3]. T. canis larvae, the cause of human toxocariasis along with T. cati, migrate to various organs and thereby cause neurological, ocular or other systemic diseases in human patients[9, 10] During their co-evolution alongside the mammalian immune system, parasites have adopted several immunomodulatory mechanisms allowing them to prevent exaggerated pathology and thereby to facilitate a chronic, long-lasting course of infection enabling completion of their life-cycle[11,12,13]. Infection with adult A. caninum is capable of suppressing intestinal pathology in dextran sodium sulphate-induced murine colitis, which is associated with dominance of Th2-related but suppression of pro-inflammatory cytokines, and recruitment of alternatively activated macrophages and eosinophils[34]. Murine cytokine responses in the context of T. canis infection are further predominated by high levels of Th2-related cytokines such as IL-4 and IL-535, 38
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