We therefore developed a model of sequential influenza pulmonary infection followed by secondary Salmonella-induced colitis using Ifnar1–/–mice to investigate the effects of IFN-Is induced during influenza infection on intestinal host defense against Salmonella. Interestingly, we found that lung induced IFN-Is enhanced the growth of Salmonella in the inflamed gut and increased its systemic dissemination to secondary sites. The gene discussed is IFNA1; the disease is colitis.