Recently, it was found that pathogens are trapped and killed by neutrophil extracellular traps (NETs). The role of Rac small GTPases is explored in the formation of NET using neutrophils lacking Rac1, Rac2 or both isoforms. NET formation was observed in both wild-type and Rac1-null neutrophils. In contrast, NET formation was markedly impaired in cells lacking either Rac2 or both Rac2 and Rac1. The defect in NET formation in Rac2-null cells was rescued in the presence of exogenous reactive oxygen species sources, suggesting that Rac2-mediated ROS generation is required. In addition, the role of nitric oxide in NET formation is assessed. Blocking NO production with the nitric oxide synthase inhibitor L-NAME significantly reduced NET formation. Moreover, Rac2-null cells produced significantly less NO than Rac1-null cells or their wild type counterparts. Our data suggest that Rac2 is essential for NET formation via pathways involving both ROS and NO.
| Identifer | oai:union.ndltd.org:TORONTO/oai:tspace.library.utoronto.ca:1807/29592 |
| Date | 25 August 2011 |
| Creators | Lim, Byung Hyun |
| Contributors | Glogauer, Michael |
| Source Sets | University of Toronto |
| Language | en_ca |
| Detected Language | English |
| Type | Thesis |
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