AI Article Synopsis
- Transgenic mice over-expressing the Bcl-2 protein showed significantly better survival rates after cecal ligation and puncture (CLP) compared to control mice, with 100% survival in myeloid-specific hMRP8-Bcl-2 mice versus only 25% in controls.
- In experiments with T lymphocyte-specific E micro -Bcl-2 mice, survival rates were also markedly higher at 87.5% compared to 22.2% in control mice.
- The protection from CLP is linked to Bcl-2's role in enhancing neutrophil presence and reducing bacterial levels, indicating its protective effect operates independently of mature T or B lymphocytes.
Article Abstract
Transgenic mice that over-express B cell leukemia/lymphomas (Bcl)-2 in myeloid cells under control of the human MRP8 promoter (hMRP8-Bcl-2) or in T lymphocytes under the E micro promoter (E micro -Bcl-2) were compared with C57BL/6 control mice following cecal ligation and puncture (CLP). There was a significant difference in outcome between the hMRP8-Bcl-2 and control mice with 100% survival in the hMRP8-Bcl-2 mice vs 25% survival in the control mice. In separate experiments there was a significant difference between E micro -Bcl-2 and control mice with 87.5 and 22.2% survival, respectively. Adoptive transfer of CD11b-positive bone marrow cells from hMRP8-Bcl-2 or C57BL/6 mice to C57BL/6 mice subjected to CLP resulted in 100 and 0% survival, respectively. Adoptive transfer of CD11b-positive cells from either hMRP8-Bcl-2 or C57BL/6 mice to Rag-1(-/-) mice (no mature T or B cells) subjected to CLP resulted in survival of 87.5 and 12.5%, respectively. The hMRP8-Bcl-2 mice had significantly more neutrophils and fewer bacteria in the peritoneum compared with C57BL/6 mice 24 h after CLP. These experiments show that Bcl-2 over-expression is protective in CLP and that protection is independent of lymphocytes. We propose that over-expression of Bcl-2 in T cells or myeloid cells induce release of a molecule(s) that protects against death following CLP.
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| http://dx.doi.org/10.4049/jimmunol.171.6.3136 | DOI Listing |
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