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dc.contributor.advisorBallinger, Megan
dc.creatorSethuraman, Shruthi
dc.description.abstractIdiopathic pulmonary fibrosis (IPF) is a fatal disease characterized by excessive collagen deposition in the lungs which can lead to death caused by respiratory failure. There is no cure for IPF, and the average life span after diagnosis is 3-5 years. Fibroblasts, the main effector cell of pulmonary fibrosis, are responsible for producing the excessive collagen deposition in the lung. Recent work has described an important role for macrophages in regulating the development and propagation of pulmonary fibrosis. Macrophages are circulating innate immune cells whose main functions are to take up pathogens or debris and secrete cytokines or chemokines. Recent work has demonstrated that macrophages isolated from IPF patients are alternatively activated and express different genes when compared to macrophages isolated from normal, donor controls. The purpose of this study is to examine crosstalk between fibroblasts and macrophages and elucidate the mechanism by which macrophages regulate collagen expression in fibroblasts.en_US
dc.publisherThe Ohio State Universityen_US
dc.relation.ispartofseriesThe Ohio State University. Department of Microbiology Honors Theses; 2019en_US
dc.subjectLung diseaseen_US
dc.titleMacrophage and Fibroblast Interaction in the Setting of Idiopathic Pulmonary Fibrosisen_US
dc.description.embargoNo embargoen_US
dc.rights.ccAttribution-NonCommercial-NoDerivs 3.0 United States*
dc.description.academicmajorAcademic Major: Microbiologyen_US

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