IP-10 is a chemokine of innate immunity, and macrophages and dendritic cells are the principal cell source. We found a higher level of IP-10 in nvA(H1N1)-mild disease, nvA(H1N1)-ARDS and bacterial-ARDS groups versus the control group, and no other differences between groups. In the nvA(H1N1)-ARDS group, the IP-10 level is higher at admission than 3 days after admission because of the survivors' cytokine profile. An increased level of IP-10 was found in the Spanish group as early response to nvA(H1N1) infection in both hospitalized and mild patient disease, as in the present study, while in the Hong Kong group IP-10 was significantly higher in critical patients only. In our study, IP-10 levels in nvA(H1N1)-ARDS nonsurvivors remained higher at admission and 3 days later, being not significantly correlated with the clinical outcome. Emphysema was one of our hystopathological findings and thus it might be speculated that a high level of IP-10 in nonsurvivors could be correlated with emphysema. IP-10 released by lung CD41 and CD81 T cells stimulates alveolar macrophage production of matrix metalloproteinase-12, which digests lung elastin [28, 29] .