In viral infections innate immune responses are initiated when viruses or their genetic material is recognized by cellular pattern recognition receptors (PRRs) of the innate immune system [1] . This recognition results in an interferon (IFN)-a/b-mediated antiviral response, as well as activation of pro-inflammatory response and programmed cell death, apoptosis, of infected cells. PRRs involved in activation of antiviral response include Toll-like receptors (TLRs) and Retinoic acid-inducible gene I-like receptors (RLRs) and the coordinated activation of TLRs and RLRs results in proper activation of antiviral response during influenza A virus infection [2, 3] . Influenza A virus infection of human macrophages also results in production of pro-inflammatory cytokines IL-1b and IL-18 [4, 5] . Both of these cytokines have to be cleaved by cysteine protease caspase-1 to generate the secreted, biologically active forms of these cytokines [6] . Caspase-1 is in turn activated in a cytosolic protein complex called inflammasome [7] . The inflammasomes consist of an adapter molecule called apoptosisassociated speck-like protein containing a caspase recruitment domain (ASC) and a PRR that belongs to either the nucleotidebinding and oligomerization domain like receptors (NLRs) or the PYHIN receptor gene family. Caspase-1 activating structures include NLRP3, NOD2/NLRP1, NOD2/NLRP3, IPAF/NAIP5, and AIM2 inflammasomes [8, 9] . Recent studies in experimental mice models have shown a critical role of NLRP3 inflammasome in the host response against influenza A virus infection [10] [11] [12] . These studies highlight the importance of IL-1b and IL-18 as mediators of host response to influenza A virus infection. However, the exact mechanism of inflammasome activation during viral infection is not known.