Abstract
The pandemic influenza A (H1N1) virus emerged in 2009 and spread globally. This virus infection can induce acute respiratory distress syndrome (ARDS) in some patients. So far, the immunophenotype of the inflammatory cells in the lung parenchyma of these patients is incompletely characterized. We have previously shown an increase of dendritic cells, natural killer cells and CD8+T cells in H1N1 patients compared to ARDS and controls patients. In the present study we extended our analysis to quantify CD4+T cells, Granzyme B, IL-17 and B lymphocytes (CD20) in the lungs of patients who died of H1N1.Methods: We analyzed autopsy lung tissue of 46 subjects (48±16 years, 55%male), divided in 3 groups according to cause of death: Control (non-pulmonary cause of death, n=16); ARDS (non viral infection cause of ARDS, n=14) and H1N1 (H1N1 infection, n=16). Using immunohistochemistry and image analysis we quantified the density of the inflammatory cells in the lung parenchyma. Results: We found an increase of CD4+ in H1N1 group when compared to ARDS and control groups (1[0,9] X 0,4[0.8] 1,4[1,8], 103cels/μm, p <0,05, respectively). The expression of Granzyme B, IL-17 and CD20, was not different between groups. Foxp3+ cells were scarcely present, and therefore not quantified. In conclusion, H1N1 virus infection is associated with an inflammatory phenotype in the alveolar region that is different from other causes of ARDS, with increased recruitment of T lymphocytes, dendritic cells and NK cells to the lungs.
- Copyright ©ERS 2015