The response of alveolar macrophages was different in a several ways from that reported for human monocyte derived macrophages. The major difference is that alveolar macrophages infected with human influenza viruses do not release much infectious virus, whereas human monocyte-derived macrophages do ( [19, 20] and Figure 3 ). The mechanism for the non-productive infection was not investigated in this study and is likely complicated. One of the possible mechanisms might be related to the lack of gene expression of transmembrane protease serine S1 member 2 (TMPRSS2) and human airway trypsin-like protease (HAT) by human AM (microarray data not shown). Both TMPRSS2 and HAT are type II transmembrane serine proteases [47] possessing trypsin-like activity and are known to be important for cleaving influenza HA required for productive infection [48] . In recent studies Bottcher et al suggest that TMPRSS2 is mainly responsible for cleavage of newly synthesized HA, whereas HAT cleaves both endocytosed and newly synthesized HA [49] . Therefore, lack of these two gene products in human AM may partially explain the lack of released infectious virus by these cells. In addition, both PR/8 and NY/238 viruses induced an early activation of type I IFN, especially IFN-a (Table 1 and Figures 1,  3, and 4) . The strong anti-viral property of type I IFN [50] may also contribute to the non-productive infection in these cells. Further studies will be required to understand the mechanism for the failure of release of infectious viral particles by human AM. In addition, inactivation of influenza by UV did not abolish the influenza viruses-stimulated CXCL10 secretion by AM (Figures 3  and 4) , which is different from studies with human monocytederived macrophages [21, 51] and with human alveolar type II epithelial cells isolated from the same donors ( [34] and data not shown). In those studies, release of CXCL10 is totally dependent on viral replication. The mechanism for the distinct CXCL10 response in human AM will require additional and carefully designed studies. The differences between human AM and monocyte-derived macrophages indicate the importance of investigating the response of AM to influenza infection during the initial phases of infection in the lung because AM are main targets for both human and avian influenza viruses [19] .