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Please use this identifier to cite or link to this item: http://hdl.handle.net/11375/23395
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dc.contributor.advisorAsk, Kjetil-
dc.contributor.authorPatel, Hemisha-
dc.date.accessioned2018-10-17T17:28:29Z-
dc.date.available2018-10-17T17:28:29Z-
dc.date.issued2018-
dc.identifier.urihttp://hdl.handle.net/11375/23395-
dc.description.abstractAn estimated 45% of all deaths can be attributed to various chronic fibroproliferative diseases. Idiopathic pulmonary fibrosis (IPF) is the most common form of interstitial lung disease which is characterized by progressive decline in lung function. While the pathogenesis of IPF is not fully understood, alternatively activated macrophages (M2) have been implicated as a key contributor to the fibrotic process. The plasticity of macrophages in vivo challenges the ability to specifically target the M2 macrophage phenotype across species. Previous bioinformatic analysis from our lab identified Dectin-1/Clec7a as a unique marker of M2 macrophages in both human and murine model systems. The expression of the transmembrane receptor Dectin-1 has not been elucidated in the context of pulmonary fibrosis. To prevent the progression of fibrosis by targeting alternatively activated macrophages, we investigated the expression of Dectin-1 in IPF and an experimental model of fibrotic lung disease. Our data demonstrated that while protein expression of Dectin-1 was increased in archived lung tissues of patients with IPF, mRNA expression of this receptor was downregulated in the tissues of these IPF patients. Gene expression of Dectin-1 was shown to be increased in monocyte-derived macrophages, further suggesting a circulatory component contributing to lung fibrosis. As expected, we confirmed that Dectin-1 was highly expressed past the injury phase of the bleomycin-model of induced pulmonary fibrosis which aligns with the increased immune infiltrates at this time point. Preliminary work into the time dependency of the resolution phase of the bleomycin-induced model of lung fibrosis was shown. All in all, our data suggests that Dectin-1 may be a useful marker in characterizing and differentiating phenotypes of macrophages implicated in the fibrotic process. Future efforts aim to gain insight into the functional requirement of Dectin-1 in the alternative activation of profibrotic macrophages to identify novel therapeutic targets for fibrotic lung disease.en_US
dc.language.isoenen_US
dc.subjectinterstitial lung diseasesen_US
dc.subjectmacrophagesen_US
dc.subjectalternatively activated macrophagesen_US
dc.subjectidiopathic pulmonary fibrosisen_US
dc.subjectdectin-1en_US
dc.subjectclec7aen_US
dc.subjectfibrosisen_US
dc.titleInvestigating the Role of Dectin-1 as a Marker of Profibrotic Macrophages in the Progression of Pulmonary Fibrosisen_US
dc.title.alternativeAlternatively activated macrophage markers and idiopathic pulmonary fibrosisen_US
dc.typeThesisen_US
dc.contributor.departmentMedical Sciencesen_US
dc.description.degreetypeThesisen_US
dc.description.degreeMaster of Science (MSc)en_US
Appears in Collections:Open Access Dissertations and Theses

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