Abstract
The peptide neuromedin B (NMB) and its receptor (NMBR) represent a system (NMB/NMBR) of neuromodulation. Here, it was demonstrated that the expression of NMBR in cells or murine lung tissues was clearly upregulated in response to H1N1/PR8 influenza A virus infection. Furthermore, the in vitro and in vivo activities of NMB/NMBR during PR8 infection were investigated. It was observed that A549 cells lacking endogenous NMBR were more susceptible to virus infection than control cells, as evidenced by the increased virus production in the cells. Interestingly, a significant decrease in IFN-α and increased IL-6 expression were observed in these cells. The role of this system in innate immunity against PR8 infection was probed by treating mice with NMB. The NMB-treated mice were less susceptible to virus challenge, as evidenced by increased survival, increased body weight, and decreased viral NP expression compared with the control animals. Additionally, the results showed that exogenous NMB not only enhanced IFN-α expression but also appeared to inhibit the expression of NP and IL-6 in PR8-infected cells and animals. As expected, opposing effects were observed in the NMBR antagonist-treated cells and mice, which further confirmed the effects of NMB. Together, these data suggest that NMB/NMBR may be an important component of the host defence against influenza A virus infection. Thus, these proteins may serve as promising candidates for the development of novel antiviral drugs.
Highlights
Influenza A viruses (IAVs) invade the respiratory tract, causing direct damage via viral replication and indirect damage via the host’s excessive defensive, production of inflammatory cytokines, called the cytokine storm [1]
Expression of neuromedin B (NMB) and neuromedin B recep‐ tor (NMBR) is upregulated in 293T and A549 cells following PR8 infection To determine the role of NMB and its receptor, NMBR, in the host antiviral response to IAV infection, the expression of NMB and NMBR was analysed in 293T and A549 cells at 0, 3, 6, 9, and 12 hpi
These results indicated that PR8 infection can significantly induce the expression of NMBR in host cells
Summary
Influenza A viruses (IAVs) invade the respiratory tract, causing direct damage via viral replication and indirect damage via the host’s excessive defensive, production of inflammatory cytokines, called the cytokine storm [1]. Cytokine dysregulation contributes to the pathogenesis of H1N1, H5N1 and H7N9 viruses [2, 3] by inducing an imbalance in the host regulatory network, which results in severe complications and high mortality rates [4, 5]. The most important methods for preventing and controlling IAV are antiviral treatments and annual vaccination. Yang et al Vet Res (2019) 50:80 as promising candidates for the development of novel and potent antiviral drugs. Such members include neuromedin B (NMB), neuromedin U, and neuropeptide S. The potential antiviral efficacy of NMB warrants further investigation
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