In the present study, we also observed that CAM suppressed enhanced S. pneumoniae adhesion by RSV infection in A549 cells. The RSV-induced S. pneumoniae adhesion was mainly mediated by host PAF receptor, as indicated by that suppressed by the PAF receptor antagonist and anti-PAF receptor monoclonal antibody. The PAF receptor acts as a receptor for S. pneumoniae and H. influenzae [12] [13] [14] . Transcription of the PAF receptor gene is controlled by NF-κB [28, 29] . We confirmed it by that the RSV-induced PAF receptor expression and S. pneumoniae adhesion were suppressed by an NF-κB inhibitor, PDTC. We revealed that CAM also suppressed PAF receptor expression induced by RSV infection and S. pneumoniae adhesion to RSV-infected A549 cells. It should be caused by the suppression of by inhibiting PAF receptor expression. CAM showed more potent suppression of RSV-induced S. pneumoniae adhesion and production of proinflammatory cytokines and chemokines than fosfomycin, as we reported previously [25, 26] . Notably, CAM significantly suppressed RSV-induced IL-6 production, whereas fosfomycin did not significantly [25] . This finding may be caused by that CAM is more potent than fosfomycin; however, the actual reason for this disparity is not clear. The upregulation of PAF receptor expression and the enhanced adhesion of pathogenic bacteria, such as S. pneumoniae, to respiratory epithelial cells are considered to be a major risk factor for secondary bacterial infections after primary respiratory viral infections. CAM may suppress both secondary bacterial infections and immunological disorders induced by RSV, without suppressing viral replication. Infection with other respiratory viruses, such as human parainfluenza virus 3 [16] and rhinovirus [17] , also upregulates known receptors for the pathogenic bacteria, including PAF receptor and S. pneumoniae adhesion. On the other hand, influenza virus does not upregulate the known receptors for bacteria, whereas bacterial adhesion is increased by the infection [16] . McCullers [39] reported that influenza-induced bacterial adhesion to A549 cells was not inhibited by PAF receptor antagonist, and the PAF receptor knock-out mice did not show lower susceptibility to experimental secondary pneumonia caused by S. pneunimoae following influenza infection compared to the parent mice. Lines of evidence suggest that adherent inducing mechanisms of S. pneumoniae to host respiratory epithelial cells are varied among viruses. So CAM may not always suppress virus-induced pathogenic bacteria adhesion.