AI Summary
The article discusses how the nasal symbiont Staphylococcus epidermidis helps to restrict influenza A virus replication by creating a polyamine-deficient cellular environment in the nasal epithelium. The study found that polyamines are necessary for the life cycle of the influenza A virus and that S. epidermidis inoculation suppressed virus infection by reducing polyamine concentrations in nasal epithelial cells. S. epidermidis was shown to regulate enzymes involved in polyamine production and export, favoring the host to limit influenza virus replication.
Studies on the immune-regulatory roles played by the commensal microbes residing in the nasal mucosa consider the contribution of antiviral immune responses. Here, we sought to identify the nasal microbiome, Staphylococcus epidermidis-regulated antiviral immune responses and the alteration of polyamine metabolites in nasal epithelium. We found that polyamines were required for the life cycle of influenza A virus (IAV) and depletion of polyamines disturbed IAV replication in normal human nasal epithelial (NHNE) cells. Inoculation of S. epidermidis also suppressed IAV infection and the concentration of polyamines including putrescine, spermidine, and spermine was completely attenuated in S. epidermidis-inoculated NHNE cells. S. epidermidis activated the enzyme involved in the production of ornithine from arginine and downregulated the activity of the enzyme involved in the production of putrescine from ornithine in nasal epithelium. S. epidermidis also induced the activation of enzymes that promote the extracellular export of spermine and spermidine in NHNE cells. Our findings demonstrate that S. epidermidis is shown to be able of creating an intracellular environment lacking polyamines in the nasal epithelium and promote the balance of cellular polyamines in favor of the host to restrict influenza virus replication.
It is becoming increasingly apparent that the primary targets of respiratory viruses, including influenza viruses, are the respiratory epithelium, and that the innate immune system of the respiratory epithelium serves as