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UBC Theses and Dissertations

Role of interleukin-10 in lung repair during influenza infection Dockstader, Kristy


The mammalian lung is intricately designed for effective gas exchange. However, infections such as influenza can damage the lung tissue and can cause a critical decrease in lung performance. Influenza is a single stranded RNA virus from the Orthomyxoviridae family. Seasonal influenza outbreaks cause up to 600 deaths in Canada each year, with increased death tolls during years with pandemic strains. Influenza A virus primarily infects the epithelial cells of the respiratory system and leads to acute respiratory infections. Tissue destruction occurs both as a result of viral-mediated apoptotic pathways, and as a consequence of the cytolytic immune response that is essential to bring the infection under control. The immune system attempts to minimize damage by producing key anti-inflammatory molecules, of which Interleukin-10 (IL-10) is a particularly potent example. IL-10 is a pleotropic cytokine that not only functions as an anti-inflammatory cytokine, but has been shown to have a role in immune stimulation, increase cytoskeletal repair and aid in the recovery of epithelial integrity. We hypothesized that IL-10 may have an effect on the remodeling and repair of lung epithelium during and after influenza A virus infection. We determined that IL-10 is up-regulated in response to infection. The timing of increased IL-10 also coincided with the height of damage, inflammation and onset of repair during an influenza infection. We used a human bronchial epithelial cell line (16HBE) to develop a model to assess if IL-10 had a direct effect on epithelial repair. Preliminary data suggested that IL-10 may inhibit epithelial cell proliferation, but further research is required. Our data suggest that IL-10 does not appear to have a role in direct epithelial proliferation but could still have a role in repair. A better understanding of the signals involved in epithelial cell repair could lead to the development of novel therapies that will minimize/mitigate lung damage caused by influenza, as well as other lung diseases.

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