Kinetics of regulatory dendritic cells in inflammatory responses during Trypanosoma evansi infection

Abstract

Summary Trypanosoma evansi (T. evansi) causes a wasting disease in almost all mammals. Trypanosoma evansi infection gives rise to the inflammatory responses that contribute to the development of inflammation‐associated tissue injury. To determine what kinds of inflammatory molecules play roles in the pathogenicity of T. evansi infection, polymerase chain reaction array analysis was performed on samples from the infected and uninfected mice. The inflammatory cytokine and chemokine storm, caused mainly by macrophages, was observed. On the other hand, the expression levels of Ccl8 and Il10 in splenocytes were also markedly increased. These results suggested an augmentation in the number and activity of regulatory dendritic cells (DCs). Therefore, the kinetics of regulatory DCs in T. evansi‐infected mice were investigated. During T. evansi infection, the regulatory DCs became prevalent, with reducing the amount of inflammatory DCs. Interestingly, when the regulatory DCs were implanted into T. evansi‐infected mice, the survival was prolonged, and the expression levels of inflammatory molecules were suppressed. Taken together, these results showed that a subset of regulatory DCs acted as a potential regulator of the inflammatory responses.

Trypanosoma evansiand Surra: A Review and Perspectives on Origin, History, Distribution, Taxonomy, Morphology, Hosts, and Pathogenic Effects

“…Behind the inflammatory cytokine and chemokine storm caused mainly by macrophages in T. evansi infections, increased expression levels for Ccl8 and Il10 in splenocytes suggested an increase in the number and activity of regulatory dendritic cells (DCs). The regulatory DCs became prevalent during the progress of infection, therefore reducing the amount of inflammatory DCs, and as a potential regulator of the inflammatory responses, suggesting the use of the inflammatory responses to immunosuppress the host, but regulation to avoid irreversible pathophysiological effects [182]. …”

Prolyl oligopeptidase-like deficient Trypanosoma evansi parasites are associated with reduced interleukin-10 concentrations in vivo and in vitro

“…Mice infected with T. evansi strain L2 showed a strong up-regulation of IL-10 and CCL8 which were responsible for the expansion of regulatory dendritic cells (DCs) during the acute phase of parasite infection (Mekata et al 2012). Inoculation of mice with regulatory DCs significantly prolonged their survival rate after infection when compared with untreated controls (Mekata et al 2012).…”

“…The role of non-inflammatory IL-10 mediated responses during T. evansi infections has been studied in mice and cattle (Mekata et al 2012(Mekata et al , 2015. Mice infected with T. evansi strain L2 showed a strong up-regulation of IL-10 and CCL8 which were responsible for the expansion of regulatory dendritic cells (DCs) during the acute phase of parasite infection (Mekata et al 2012).…”

Expression of regulatory dendritic cell-related cytokines in cattle experimentally infected with <i>Trypanosoma evansi</i>

“…The cellular and molecular components that govern this delicate balance are necessary to understand the pathology of T. evansi infection. We have previously reported that regulatory dendritic cells (DCs), which secret a high dose of IL-10 and activate regulatory T cells [ 19 , 22 ], were induced in mice experimentally infected with T. evansi and controlled excessive inflammation [ 11 ]. In this study, we reveal that the phenomenon also occurs in cattle, the natural hosts of T. evansi .…”

“…[ 4 ]. Extraction of total RNA from the peripheral blood mononuclear cells (PBMCs) and quantification of the cytokines by real-time PCR were performed as described by Mekata et al [ 11 ]. We set the mean cytokine expression of one day and just before the injection of trypanosome as the reference of relative ratio.…”