In the present study, we have demonstrated a pattern of host responses in swine macrophages to H1N1pdm infection. Strong proinflammtory and antiviral cytokine responses including IL-6, IL-8, TNF-a, as well as IFN-b, were observed. In contrast, IL-1b was not induced, and was barely detectable in pig macrophages. This pattern differs from that in bronchoalveolar secretions of SIV-infected pigs in which IL-1b was induced but IL-8 was not [19, 20, 21, 22, 25] . The different cell types involved (macrophages and epithelial cells) may account for the difference. It has previously been reported that in human immune cells and patients a weak innate immune response, evidenced by a poor induction of proinflammatory and antiviral cytokines including IFN-b and TNF-a, has been observed in human monocyte-derived DCs and macrophages infected with H1N1pdm, compared to seasonal H1N1 infection [31] . Highly pathogenic H5N1 viral infection in human macrophages induced higher expression of IL-6 and CCL5 (RANTES) than pH1N1 [32] , which may explain generally mild clinical disease among H1N1pdm-infected patients. In human macrophages, similar to our findings, IL-1b was not detected.