Abstract
Neospora caninum is an apicomplexan parasite that in cattle assumes particular importance, as it is responsible for abortions reported worldwide. Leptin is an adipokine mainly secreted by adipocytes, which beside its role in maintaining metabolic homeostasis also has important effects in both innate and adaptive immunity. In previous work, we showed that mice chronically infected with N. caninum had elevated serum leptin levels. Here, we sought to assess whether acute infection with N. caninum infection influenced the production of this adipokine as well as leptin receptor mRNA levels. Our results show that acute infection with N. caninum led to decreased leptin serum levels and mRNA expression in adipose tissue. A decrease in leptin receptor transcript variant 1 mRNA (long isoform) and leptin receptor transcript variant 3 mRNA (one of the short isoforms) expression was also observed. An increase in the number of cells staining positive for leptin in the liver of infected mice was observed, although this increase was less marked in Interleukin (IL)-12/IL-23 p40-deficient mice. Overall, our results show that N. caninum infection also influences leptin production during acute infection.
Highlights
Neospora caninum is an apicomplexan parasite, phylogenetically close to Toxoplasma gondii, that was first described as a causative agent of neurologic disease in dogs [1,2]
Our results show that acute infection with N. caninum led to a decrease in the levels of leptin that was accompanied by decreased leptin receptor expression in adipose tissue
No differences in the weight of inguinal subcutaneous adipose tissue (SAT), gonadal adipose tissue (GAT), and mesenteric adipose tissue (MAT) were observed between infected and phosphate-buffered saline (PBS) control groups (Figure 1b)
Summary
Neospora caninum is an apicomplexan parasite, phylogenetically close to Toxoplasma gondii, that was first described as a causative agent of neurologic disease in dogs [1,2]. Bovine neosporosis leads to heavy economic losses in the dairy and beef industry, and no vaccine exists to prevent this infection [3,4]. Mice genetically deficient for these cytokines [5,6] or mice in which these cytokines were neutralized with specific monoclonal antibodies [7] were shown to be lethally susceptible to N. caninum infection. Our latest work uncovered noticeable immune cell alterations occurring in the adipose tissue during N. caninum infection that persisted long after local parasite elimination [8,9]. Distinct lymphoid cell populations, such as CD4+ and CD8+ TCRβ+ cells, TCRγδ+ cells and Pathogens 2020, 9, 587; doi:10.3390/pathogens9070587 www.mdpi.com/journal/pathogens
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