Exploring the TLR and NLR signaling pathway relevant molecules induced by the Theileria annulata infection in calves
Theileria annulata is the pathogen of bovine tropical theileriosis. It is extremely harmful to the cattle industry, with huge economic losses. The toll-like receptor (TLR) and NOD-like receptor (NLR) signaling pathways are crucial for resistance to infection of the protozoa, such as Plasmodium falciparum, Toxoplasma gondii, and Trypanosoma cruzi. However, the role of these immune-related pathways is unclear during T. annulata infection. In the present study, peripheral blood mononuclear cells and serum were separated from blood samples of calves infected with homogenized tick supernatants carrying T. annulata sporozoites at 12 h, 24 h, 36 h, 48 h, 72 h, 96 h, 120 h, 144 h and 168 h postinoculation. The Custom RT2 Profiler PCR Array was used to explore the mRNA levels of 42 TLR and NLR signaling pathway relevant genes. The TLR1, TLR6, TLR10, NLRP1, and MyD88 genes and their downstream signaling molecules significantly differed after the T. annulata infection in comparison with that of preinfection from 72 h to 168 h postinoculation. The serum concentrations of IL-6, IL-1β, and TNFα were significantly increased at 96 h and 168 h postinfection. These findings provided novel information to help determine the mechanisms of TLR and NLR signaling pathway involvement in protection against T. annulata infection.
KeywordsTheileria annulata Innate immunity TLRs NLRs PCR array
This study was supported by the National Key Basic Research Program (973 program) of China (No. 2015CB150300); the National Key Research and Development Program of China (No. 2017YFD0501200); ASTIP, FRIP (No. 2014ZL010), CAAS; NBCIS CARS-38; NSFC (No. 31372432, 31,402,189); and Jiangsu Co-innovation Center Programme for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, State Key Laboratory of Veterinary Etiological Biology Project. The research was also facilitated by CRP No. 16198/R0 IAEA.
Compliance with ethical standards
The authors declare that they have no competing interests.
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