Acute Respiratory Distress Syndrome is a late cause of morbidity and mortality following hemorrhagic shock and resuscitation. Previous work in our laboratory showed that alveolar macrophages were primed for increased responsiveness to lipopolysaccharides, as evidenced by augmented inflammatory cytokine production.
Recent studies have shown that macrophages can be polarized into two phenotypes, namely pro-inflammatory M1 and anti-inflammatory M2 macrophages, in response to various environmental cues. The major hypothesis to be tested in this thesis is that HS/R shifts the M1/M2 polarization of alveolar macrophages to favour a pro-inflammatory milieu in the lung.
A biphasic shift in the phenotype of alveolar macrophages in response to HS/R characterized by an early reduction of M2 cells followed by a late up-regulation of M1 macrophages was observed. The administration of M2- polarizing PPARγ agonists prior to HS/R restored the M1/M2 balance of alveolar macrophages and reduced lung injury.
| Identifer | oai:union.ndltd.org:TORONTO/oai:tspace.library.utoronto.ca:1807/43858 |
| Date | 18 February 2014 |
| Creators | Dana, Safavian |
| Contributors | Ori, Rotstein |
| Source Sets | University of Toronto |
| Language | en_ca |
| Detected Language | English |
| Type | Thesis |
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