Cytokine profiles of suction pulmonary secretions from children infected with pandemic influenza A(H1N1) 2009

uenza in humans is characterized by massive virus replication in respiratory epithelial cells, infl ammation and an abrupt onset. Th e novel infl uenza A (H1N1) 2009 caused an epidemic of critical illness and some patients rapidly developed severe acute respiratory distress syndrome [1,2]. Van Reeth [3] reviewed growing evidence that the so-called early cytokines produced at the site of infection mediate many of the clinical and pathological manifestations of infl uenza infection. Of those cytokines, Bermejo-Martin and colleagues [4] reported in Critical Care that T-helper 1 (Th 1) and Th 17 hypercytokinemia plays an important role as an early host response in severe pandemic infl uenza. Evaluating the diff erences in early immune responses between hospita lized patients with severe pandemic infl uenza and those with mild disease, high systemic levels of IFN-γ and a group of mediators involved in the development of the Th 17 (IL-8, IL-9, IL-17, IL-6) and Th 1 (TNF-α, IL-15, IL-12p70) responses were found exclusively in hospitalized patients. A signifi cant inverse association was found between IL-6 and IL-8 and PaO2 in critical patients. Th ey concluded that severe disease with respira tory involvement is characterized by early secretion of Th 17 and Th 1 cytokines. We experienced two cases of pandemic infl uenza A(H1N1) 2009-associated pneumonia and encephalopathy, which were treated under mechanical ventilation. Cytokine analysis of their pulmonary secretions revealed diff erent patterns from previous results (Figure 1). One patient showed no improvement with usual ventilation and had mediastinal emphysema and serious hypooxygenation; thus, the patient needed to be ventilated using the special respiratory airway pressure release ventilation mode because of progression and the need for high pressure control. Th e second case with encephalopathy compli cated with pneumonia underwent combined treatments of steroids and hypothermia because of intractable recurrent seizures. Th eir cytokine levels were extremely high, although serum 17 cytokines were within normal ranges. Cytokines in pulmonary secretions at fi rst revealed high levels of IL-8, monocyte chemotactic protein (MCP)-1 and macrophage infl ammatory protein1b (MIP-1b). On the other hand, IL-1b, 2, 4, 5, 6, 7, 10, 12, 13, 17, G-CSF, GM-CSF, IFN-γ and TNF-α were normal or slightly increased. On 5th days after hospitalization other cytokines (IL-1β, 6, 10, 17, G-CSF, GM-CSF, IFN-γ, MCP-1 and TNF-α) increased markedly in both cases. Given these fi ndings, we suspect that