Although both instruments proved to be useful in this study, the performance of AMSTAR in terms of reliability and validity was better than OQAQ; the new tool is reliable, valid, and easy to use when applied to assess methodological quality of systematic reviews on TCM, although there is room for improvement on a few items. Innate Immune Response of Human Alveolar Macrophages during Influenza A Infection Alveolar macrophages (AM) are one of the key cell types for initiating inflammatory and immune responses to influenza virus in the lung. However, the genome-wide changes in response to influenza infection in AM have not been defined. We performed gene profiling of human AM in response to H1N1 influenza A virus PR/8 using Affymetrix HG-U133 Plus 2.0 chips and verified the changes at both mRNA and protein levels by real-time RT-PCR and ELISA. We confirmed the response with a contemporary H3N2 influenza virus A/New York/238/2005 (NY/238). To understand the local cellular response, we also evaluated the impact of paracrine factors on virus-induced chemokine and cytokine secretion. In addition, we investigated the changes in the expression of macrophage receptors and uptake of pathogens after PR/8 infection. Although macrophages fail to release a large amount of infectious virus, we observed a robust induction of type I and type III interferons and several cytokines and chemokines following influenza infection. CXCL9, 10, and 11 were the most highly induced chemokines by influenza infection. UV-inactivation abolished virus-induced cytokine and chemokine response, with the exception of CXCL10. The contemporary influenza virus NY/238 infection of AM induced a similar response as PR/8. Inhibition of TNF and/or IL-1β activity significantly decreased the secretion of the proinflammatory chemokines CCL5 and CXCL8 by over 50%. PR/8 infection also significantly decreased mRNA levels of macrophage receptors including C-type lectin domain family 7 member A (CLEC7A), macrophage scavenger receptor 1 (MSR1), and CD36, and reduced uptake of zymosan. In conclusion, influenza infection induced an extensive proinflammatory response in human AM. Targeting local components of innate immune response might provide a strategy for controlling influenza A infection-induced proinflammatory response in vivo. Alveolar macrophages (AM) reside at the air-tissue interface in the lung and are one of the first lines of defense that interact with inhaled microorganisms and particles [1] . They play a critical role in homeostasis, host defense, and tissue remodeling [2] , and they are readily infected by influenza [3] . AM express many pattern recognition receptors (PRRs) to help recognize the pathogenassociated molecular patterns (PAMPs) on the surface of microorganisms [4, 5] . They are important in initiating response to influenza, regulating the inflammatory response, and potentially limiting secondary bacterial infections [6] .