Altogether, the PR8-induced upregulation of VCAM-1 expression on the lung vascular endothelium and the capacity of PR8 to stimulate a similar number of lung MCp in the chimeric mice and in normal non-irradiated mice strongly suggest that the major mechanism behind the influenza-induced increase in MCp numbers is recruitment of blood MCp to the lung. This evidence concerns the gene VCAM1 and influenza.