Studies have been conducted to identify proinflammatory cytokines including TNF-a, IL-6, IL-12, and IFN-a or IFN-c, which are upregulated in lung or bronchoalveolar secretions in SIV-infected pigs [18, 19, 20, 21] and may be correlated with clinical manifestations. In an alveoli macrophage-depleted pig model, macrophages appeared to be indispensible to effective clearance of SIV from lungs. A higher frequency of cytotoxic T, cd T, and Treg cells were also detected in infected pig lungs [18] , which together with the induction of cytokines, contribute to pathogenesis of influenza infection in pigs. Exploring the mechanism of regulation of host responses is crucial for understanding the pathogenesis of SIV and for controlling swine influenza in pigs. Macrophages residing beneath the respiratory epithelium and surrounding alveoli are part of the first line defenses against influenza viruses. During influenza viral replication in bronchial epithelial cells, macrophages are one of the earliest targets to be infected. Together with dendritic cells, macrophages coordinate innate immune responses, which subsequently lead to adaptive immunity by initiating antigen presentation and lymphocyte activation. Macrophages are indispensable in alveolar host defense and controlling influenza virus in pulmonary organs in pigs [22] . While protective in launching host antiviral responses and restricting virus spread, induced proinflammatory cytokines and chemokines are also the cause of pathogenicity for the host and may lead to acute respiratory failure (ARF), a major cause of death in highly pathogenic H5N1 or H1N1pdm-infected humans [23] . Needless to say, the roles of macrophages are critical to pathogenicity as well as host protection in SIV-infected pigs. However, little is known about the mechanisms of how host responses are regulated in pigs or their macrophages.