In contrast, except the bacterial-ARDS group presented no lymphocytopenia, lower elevation in serum liver enzymes and higher levels of C-reactive protein and procalcitonin. No significant differences were found between bacterial and viral ARDS groups in SOFA and APACHE II scores at admission. The pulmonary histopathological findings in nvA(H1N1)-ARDS nonsurvivors were similar to other fatal cases of nvA(H1N1) virus infection [12,13].Installation of ARDS in the course of the disease was the moment of blood sampling for cytokine measurements. There was a difference regarding the time of symptom onset and hospital admission between the severe and mild groups of nvA(H1N1) disease that could affect the comparison of cytokine levels between the two groups.

For this reason we not only compared the cytokine levels between mild and severe disease, but also mixed the patients with nvA(H1N1)-mild and severe disease and compared the level of cytokines according to the interval between symptom onset and admission (first interval 1 to 5 days, second interval 6 to 14 days). We found that not all cytokines had the same behavior against the time of symptom onset and admission.The pattern of immune response in patients with nvA(H1N1) virus infection is incompletely characterized. CD4+ T cells are known to play an important role in the initiation of immune responses by providing help to other cells. T-helper cells could be divided into subsets: Th1, Th2 and Th17.Th1 cells mainly develop following infections by intracellular bacteria and some viruses [14].

The mediators involved in the development of Th1 are IL-12, IFN��, IL-15, IL-18 and TNF��.IL-12 bridges the early nonspecific innate immunity and the subsequent antigen-specific adaptative immunity [15]. IL-12 was shown to inhibit apoptosis of T cells [16] and of dendritic cells [17]. Alveolar macrophages have a functional IL-12 receptor, and virus-infected macrophages in the presence of IL-12 might be protected from apoptosis limiting viral clearance [18]. Apoptosis of virus-infected cells was shown to be an effective mechanism for viral clearance [19]. Bermejo-Martin and colleagues reported more significant IL-12 results in the critical A(H1N1) group of patients [9]. In our study, IL-12 is significantly higher in the nvA(H1N1)-mild disease group and in the nvA(H1N1)-ARDS group versus the control group and is not significantly higher in the bacterial ARDS group.

IL-15 plays a critical role in protecting CD8+ T cells from apoptosis during the contraction phase following microbial AV-951 infection [20,21]. The CD8+ T cells surviving in the presence of IL-15 might be pathogenic in lung injury following highly pathogenic influenza A virus infection [22]. IL-15 activates the effector function of memory phenotype CD8+ cells [23].