Sarcocystis fusiformis is a coccidian tissue parasite that causes infection in buffalo in countries such an Egypt, China, Iraq and Iran, resulting in significant economic losses to the agricultural industry annually. There is a lack of studies examining host-parasite interactions at the level of the immune response and the present study investigates the interaction between S. fusiformis whole cyst antigens (SFWCA) and dendritic cells (DCs), cells critical to the activation of adaptive immunity. In this study bone marrow derived DCs (BMDCs) were phenotyped following treatment with SFWCA by measuring cell viability, cytokine secretion, and cell surface marker expression. While SFWCA exhibited cytotoxic effects on BMDCs at higher concentrations, lower concentrations of SFWCA activated pro-inflammatory DCs that significantly secreted interleukin (IL)-12p40, tumor necrosis factor alpha, IL-6 and IL-10. These cells also displayed enhanced expression of TLR4, CD80, CD86 and MHC II on their surface, which is indicative of full DCs maturation. Moreover, SFWCA significantly attenuated the capacity of BMDCs to suppress Th2 associated cytokines, notably IL-5 and IL-13, while simultaneously exhibiting no effects on the secretion of interferon (IFN)-c, IL-2, IL-17, and IL-10. In conclusion, this is the first study to provide fundamental insight into the activation of DCs by SFWCA, providing us with some awareness into the interaction of the Sarcosystis parasite with its host. The pro-inflammatory inducing ability of this antigen is in keeping with studies performed in other protozoan parasites and therefore understanding these interactions is important in the development of future therapeutic strategies.

Cryptosporidium parvum is an opportunistic intracellular parasite that causes disease in animal populations such as calves and goats. It is also a significant zoonotic disease globally, causing mild to severe human diarrhea. In immunocompromised animals, calves and lambs, and immunocompromised humans such as AIDS patients, an infection can be lifethreatening as no effective treatments are currently available to control infection. The effects of Cryptosporidium parvum antigen (CPA) on dendritic cells (DCs) were investigated. This study examined cytokine secretion and cell surface marker expression on DCs exposed to CPA. Cytokine production in CD4 + cells co-cultured with CPA primed DCs in the presence of anti-CD3 was also measured. CPA induced a significant increase in the production of interleukin (IL)-12p40, IL-10, IL-6, and TNF-α by DCs and enhanced the expression of the cell surface markers TLR4, CD80, CD86, and MHC11. CPA primed DC co-cultured in the presence of anti-CD3 with CD4 + T-cells inhibited the secretion of Th2-associated cytokines, notably IL-5 and IL-13, with no effects on the secretions of interferon (IFN)-γ, IL-2, IL-17, and IL-10. These findings support studies in the literature that CPA can induce the full maturation of DCs that subsequently initiate Th1 immune responses critical to the resolution of C. parvum infection.

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