angiotensin-i and Pneumococcal-Infections

Resolution failure of exacerbated inflammation triggered by Influenza A virus (IAV) prevents return of pulmonary homeostasis and survival, especially when associated with secondary pneumococcal infection. Therapeutic strategies based on pro-resolving molecules have great potential against acute inflammatory diseases. Angiotensin-(1-7) [Ang-(1-7)] is a pro-resolving mediator that acts on its Mas receptor (MasR) to promote resolution of inflammation. We investigated the effects of Ang-(1-7) and the role of MasR in the context of primary IAV infection and secondary pneumococcal infection and evaluated pulmonary inflammation, virus titers and bacteria counts, and pulmonary damage. Therapeutic treatment with Ang-(1-7) decreased neutrophil recruitment, lung injury, viral load and morbidity after a primary IAV infection. Ang-(1-7) induced apoptosis of neutrophils and efferocytosis of these cells by alveolar macrophages, but had no direct effect on IAV replication in vitro. MasR-deficient (MasR

Topics: A549 Cells; Angiotensin I; Animals; Anti-Inflammatory Agents; Bronchoalveolar Lavage Fluid; Cytokines; Dogs; Humans; Influenza A virus; Lung; Madin Darby Canine Kidney Cells; Male; Mice, Inbred C57BL; Mice, Knockout; Neutrophils; Peptide Fragments; Peroxidase; Phagocytosis; Pneumococcal Infections; Pneumonia, Viral; Proto-Oncogene Mas; Proto-Oncogene Proteins; Receptors, G-Protein-Coupled; Streptococcus pneumoniae