Tatsuya Tsukui, PhD

In pulmonary fibrosis, ongoing lung injury leads to the replacement of healthy lung tissue with scarred fibrous tissue produced by diseased fibroblasts (cells that contribute to the formation of connective tissue). This impairs lung function. Currently, there is no treatment that can reverse pulmonary fibrosis. Inflammatory responses in lung tissue trigger a series of events that promote fibrosis following injury. We recently identified different types of fibroblasts that arise from specific inflammatory signals in pulmonary fibrosis. However, the impact of these diverse inflammatory signals on the behavior of diseased fibroblasts remains unclear. We will determine the role of these inflammatory signals on fibroblasts in pulmonary fibrosis by using innovative tools, which we recently generated to specifically target fibroblast subsets. These studies will show how inflammatory signals contribute to pulmonary fibrosis and may lead to novel therapeutic strategies to target inflammatory fibroblasts.

Update: We studied how inflammatory signals affect fibroblasts and their role in controlling immune responses during lung injury and fibrosis. In earlier research, we found that alveolar fibroblasts turn into inflammatory fibroblasts early in fibrotic injury and can later become fibrotic fibroblasts. When we prevented this transformation and caused lung injury, we saw changes in the types of cytokines produced by immune cells, especially those in the innate immune system. We also found that fibroblasts influence immune responses differently depending on the type of injury, showing that they can take on different roles to support various immune reactions.