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Rapid replication of the influenza A virus and lung tissue damage caused by exaggerated pro-inflammatory host immune responses lead to numerous deaths. Therefore, novel therapeutic agents that have anti-influenza activities and attenuate excessive pro-inflammatory responses that are induced by an influenza virus infection are needed. Oligoribonucleotides-d-mannitol (ORNs-d-M) complexes possess both antiviral and anti-inflammatory activities. The current research was aimed at studying the ORNs-d-M effects on expression of innate immune genes in mice lungs during an influenza virus infection. Expression of genes was determined by RT-qPCR and Western blot assays. In the present studies, we found that the ORNs-d-M reduced the influenza-induced up-expression of Toll-like receptors (TLRs) ( tlr3 , tlr7 , tlr8 ), nuclear factor NF-kB ( nfkbia , nfnb1 ), cytokines ( ifnε , ifnk , ifna2 , ifnb1 , ifnγ , il6 , il1b , il12a , tnf ), chemokines ( ccl3 , ccl4 , сcl5 , cxcl9 , cxcl10 , cxcl11 ), interferon-stimulated genes (ISGs) ( oas1a , oas2 , oas3 , mx1 ), and pro-oxidation ( nos2 , xdh ) genes. The ORNs-d-M inhibited the mRNA overexpression of tlr3 , tlr7 , and tlr8 induced by the influenza virus, which suggests that they impair the upregulation of NF-kB, cytokines, chemokines, ISGs, and pro-oxidation genes induced by the influenza virus by inhibiting activation of the TLR-3, TLR-7, and TLR-8 signaling pathways. By impairing activation of the TLR-3, TLR-7, and TLR-8 signaling pathways, the ORNs-d-M can modulate the innate immune response to an influenza virus infection.

Complexes of Oligoribonucleotides with d-Mannitol Modulate the Innate Immune Response to Influenza A Virus H1N1 (A/FM/1/47) In Vivo