Transcription of inflammatory genes in innate immune cells is coordinately regulated by transcription factors, including NF‐κB, and chromatin modifiers. However, it remains unclear how microbial sensing initiates chromatin remodeling. Here, we show that Akirin2, an evolutionarily conserved nuclear protein, bridges NF‐κB and the chromatin remodeling SWI/SNF complex by interacting with BRG1‐Associated Factor 60 (BAF60) proteins as well as IκB‐ζ, which forms a complex with the NF‐κB p50 subunit. These interactions are essential for Toll‐like receptor‐, RIG‐I‐, and Listeria‐mediated expression of proinflammatory genes including Il6 and Il12b in macrophages. Consistently, effective clearance of Listeria infection required Akirin2. Furthermore, Akirin2 and IκB‐ζ recruitment to the Il6 promoter depend upon the presence of IκB‐ζ and Akirin2, respectively, for regulation of chromatin remodeling. BAF60 proteins were also essential for the induction of Il6 in response to LPS stimulation. Collectively, the IκB‐ζ–Akirin2–BAF60 complex physically links the NF‐κB and SWI/SNF complexes in innate immune cell activation. By recruiting SWI/SNF chromatin remodellers to IκB‐ζ, transcriptional coactivator for NF‐κB, the conserved nuclear protein Akirin2 stimulates pro‐inflammatory gene promoters in mouse macrophages during innate immune responses to viral or bacterial infection.