Cysticercus pisiformis-derived novel-miR1 targets TLR2 to inhibit the immune response in rabbits

Cysticercosis pisiformis, a highly prevalent parasitic disease worldwide, causes significant economic losses in the rabbit breeding industry. Previous investigations have identified a novel microRNA, designated as novel-miR1, within the serum of rabbit infected with Cysticercus pisiformis. In the present study, we found that C. pisiformis-derived novel-miR1 was released into the rabbit serum via exosomes. Through computational analysis using TargetScan, miRanda, and PITA, a total of 634 target genes of novel-miR1 were predicted. To elucidate the functional role of novel-miR1, a dual-luciferase reporter assay was utilized and demonstrated that novel-miR1 targets rabbit Toll-like receptor 2 (TLR2). Rabbit peripheral blood lymphocytes (PBLCs) were transfected with novel-miR1 mimic and mimic NC, and the in vitro experiments confirmed that novel-miR1 suppressed the expression of pro-inflammatory cytokines such as TNF-alpha, IL-1 beta, and IL-6 through the nuclear factor kappa B (NF-kappa B) pathway. In vivo experiments demonstrated that novel-miR1 was significantly upregulated during the 1-3 months following infection with C. pisiformis in rabbits. Notably, this upregulation coincided with a downregulation of TLR2, P65, pP65, TNF-alpha, IL-1 beta, and IL-6 in PBLCs. Collectively, these results indicate that the novel-miR1 derived from C. pisiformis inhibited the rabbits' immune response by suppressing the NF-kappa B-mediated immune response. This immune modulation facilitates parasite invasion, survival, and establishment of a persistent infection.

Automated summary

C. pisiformis-derived novel-miR1 was released into rabbit serum via exosomes and suppressed the expression of TLR2, inhibiting the immune response and facilitating parasite infection.