Abstract
Rational strategies for the treatment of burn injury and infection require an improved understanding of the mechanisms by which immune suppression and pro-inflammatory signals interact. Here we study the dynamics of granulopoiesis in the bone marrow (BM) using a mouse burn/infection model to identify the roles that apoptosis, differentiation, proliferation and release play in the etiology of the immunologic response to burns and superimposed infection. We demonstrate that there is a rapid loss of mature granulocytes (CD11b+ Ly6G+) from the marrow during a primarily septic injury using a clinical isolate of Pseudomonas aeruginosa (PA-14). Due to the short timescale involved massive and specific release of granulocytes from the marrow is the most likely mechanism for the observed dynamics. There is also clear evidence of a drop in the bone marrow cellularity for animals with superimposed burn and sepsis. Using a simple population balance approach we demonstrate that a decreased cell residence time in the mature bone marrow pool could explain the observed rapid decline in its size.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 796-797 |
| Number of pages | 2 |
| Journal | Annual International Conference of the IEEE Engineering in Medicine and Biology - Proceedings |
| Volume | 1 |
| State | Published - 2002 |
| Externally published | Yes |
| Event | Proceedings of the 2002 IEEE Engineering in Medicine and Biology 24th Annual Conference and the 2002 Fall Meeting of the Biomedical Engineering Society (BMES / EMBS) - Houston, TX, United States Duration: Oct 23 2002 → Oct 26 2002 |
All Science Journal Classification (ASJC) codes
- Signal Processing
- Biomedical Engineering
- Computer Vision and Pattern Recognition
- Health Informatics
Keywords
- Bone marrow
- Burn injury
- Granulopoiesis
- Sepsis