Radix Isatidis polysaccharide (RIP) resists the infection of QX-type infectious bronchitis virus via the MDA5/TLR3/IRF7 signaling pathway

Although vaccines play a major role in the prevention of infectious bronchitis (IB), Anti-IB drugs still have great potential in poultry production. Radix Isatidis polysaccharide (RIP) is a crude extract of Banlangen with antioxidant, antibacterial, antiviral, and multiple immunomodulatory functions. The aim of this study was to explore the innate immune mech-anisms responsible for RIP-mediated alleviation of infectious bronchitis virus (IBV)-induced kidney lesions in chickens. Specific-pathogen-free (SPF) chicken and chicken embryo kidney (CEK) cells cul-tures were pretreated with RIP and then infected with the QX-type IBV strain, Sczy3. Morbidity, mortality, and tissue mean lesion scores were calculated for IBV-infected chickens, and the viral loads, inflammatory factor gene mRNA expression levels, and innate immune pathway gene mRNA expression levels in infected chickens and CEK cell cultures were deter-mined. The results show that RIP could alleviate IBV-induced kidney damage, decrease CEK cells sus-ceptibility to IBV infection, and reduce viral loads. Additionally, RIP reduced the mRNA expression levels of the inflammatory factors IL-6, IL-8, and IL-1/3 by decreasing the mRNA expression level of NF-kB. Conversely, the expression levels of MDA5, TLR3, STING, Myd88, IRF7, and IFN-/3 were increased, indi-cating that RIP conferred resistance to QX-type IBV infection via the MDA5, TLR3, IRF7 signaling path-way. These results provide a reference for both further research into the antiviral mechanisms of RIP and the development of preventative and therapeutic drugs for IB.

Automated summary

This study aimed to explore the effects and mechanisms of Radix Isatidis polysaccharide (RIP) on kidney damage caused by infectious bronchitis virus (IBV) in poultry. The results showed that RIP could alleviate virus-induced kidney damage, reduce cell susceptibility to virus infection, and decrease viral loads. RIP also regulated the expression of inflammatory factors and immune pathway genes, enhancing resistance to IBV infection.