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.
- 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].
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.
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Cat. No.Product NameDescriptionTargetResearch Area
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target: NF-κB
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