Cryptosporidium parvum downregulates miR-181d in HCT-8 cells via the p50-dependent TLRs/NF-κB pathway

  • Vet Parasitol. 2022 May;305:109710. doi: 10.1016/j.vetpar.2022.109710.
Ruiying Feng  1 Ziwen Niu  1 Xiaotian Zhang  1 Wenyan Hou  1 Yingying Zhang  1 Fuchun Jian  1 Changshen Ning  1 Longxian Zhang  1 Sumei Zhang  2 Rongjun Wang  3
Affiliations
  • 1. College of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450046, China; International Joint Research Laboratory for Zoonotic Diseases of Henan, Zhengzhou 450046, China.
  • 2. College of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450046, China; International Joint Research Laboratory for Zoonotic Diseases of Henan, Zhengzhou 450046, China. Electronic address: [email protected].
  • 3. College of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450046, China; International Joint Research Laboratory for Zoonotic Diseases of Henan, Zhengzhou 450046, China. Electronic address: [email protected].
Abstract

Cryptosporidium spp. can cause diarrhea and even death in humans and Animals. Host MicroRNAs (miRNAs) play an important role in the post-transcriptional regulation of the innate immune response to Cryptosporidium Infection. To study host miRNA activity in the innate immune response to C. parvum Infection, we examined the expression of miR-181d in HCT-8 cells infected with C. parvum and found that it was significantly downregulated, while TLR2, TLR4, NF-κB, and MyD88 involved in the TLR/NF-κB signaling pathway were significantly upregulated at the early stages of C. parvum Infection. We transfected cells with short-interfering RNAs (siRNA) as TLR2, TLR4, and NF-κB inhibitors. Analysis by quantitative real-time polymerase chain reaction (qPCR) and western blot confirmed that C. parvum downregulates miR-181d expression via the p50 subunit-dependent TLR2/TLR4-NF-κB signaling pathway in HCT-8 cells. This study provides a new theoretical foundation to elucidate the regulatory mechanism of host miRNAs against Cryptosporidium Infection.

Keywords
Cryptosporidium parvum; HCT-8; MiR-181d; NF-κB; TLRs.
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