Proper regulation of apoptosis during pneumococcal pneumonia is essential for resolution of infection. We hypothesized that reactive oxygen species (ROS) produced during infection causes sufficient DNA damage to alter expression of pro-apoptotic proteins. Despite inducing DNA damage, challenge with pneumococci did not cause alterations the expression of the pro-apoptotic protein Puma (p53 up-modulated regulator of apoptosis) at early (4 and 6 hour) and late (16 and 24 hour) time points tested in this study. Puma-dependent global expression patterns were assessed, and the data demonstrated significant changes in expression of various genes (Prdx2, Ripk1, Api5 and IL-10) involved in cell death and the inflammatory response. In conclusion, although the presence of Puma is necessary for normal apoptotic cellular death and host resolution of infection, Puma expression in bone marrow neutrophils and lung epithelial cells is not dependent on ROS produced during pneumococcal infection.
| Identifer | oai:union.ndltd.org:MSSTATE/oai:scholarsjunction.msstate.edu:td-3187 |
| Date | 11 May 2013 |
| Creators | Jones, Andrea Rodgers |
| Publisher | Scholars Junction |
| Source Sets | Mississippi State University |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | Theses and Dissertations |
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