IL-6 is a cytokine of innate immunity, its principal targets being the liver cells, the β cells and the naïve T cells [25] . Despite the apparently beneficial role that macrophages play in controlling early viral replication, several reports have demonstrated a more deleterious effect of these cells in influenza A viral infections by excessive inflammation in the lung attributed to IL-6 and TNFα [26] . In our study, IL-6 is increased in nvA(H1N1)-ARDS versus nvA(H1N1)-mild disease. Similarly, IL-6 and IL-15 constituted a hallmark of critical illness in the Hong Kong and Spanish nvA(H1N1) cytokine studies [8, 9] . In the nvA(H1N1)-ARDS group, the IL-6 serum level is significantly higher at admission than 3 days later. In the same group, IL-6 is significantly higher in nonsurvivors versus survivors at admission and 3 days later, which seems to further contribute to pulmonary damage and death. We found positive correlations between IL-6, IL-15 and IL-8 levels and a longer than 5 days interval between symptom onset and admission, as well as with C-reactive protein, but a negative correlation with the PaO 2 :FiO 2 ratio, indicating the severity of the disease. IL-8 is a chemokine of innate immunity. The chemokine's principal biologic effect is chemotaxis, being a major chemokine for neutrophil activation, and migration into tissues [24] . In our study, IL-8 is highly significant in the nvA(H1N1)-ARDS and ARDS bacterial groups versus the control group, but is not significant in mild disease. In contrast, IL-8 was increased in both critical and noncritical nvA(H1N1) hospitalized patients in the Spanish and Hong Kong studies. In our study, IL-8 is higher in nvA(H1N1)-ARDS versus nvA(H1N1)-mild disease and in bacterial ARDS versus nvA(H1N1)-ARDS. The obese patients with nvA(H1N1) disease had a significant level of IL-8. Plasma IL-8 levels are increased in normoglycemic obese subjects, related to fat mass and the TNFα system [27] .