| Autor: |
Tschöp, Johannes, Martignoni, André, Goetzman, Holly S., Choi, Lisa G., Wang, Quan, Noel, John G., Ogle, Cora K., Pritts, Timothy A., Johannigman, Jay A., Lentsch, Alex B., Caldwell, Charles C. |
| Zdroj: |
Journal of Leukocyte Biology; March 2008, Vol. 83 Issue: 3 p581-588, 8p |
| Abstrakt: |
Sepsis is a difficult condition to treat and is associated with a high mortality rate. Sepsis is known to cause a marked depletion of lymphocytes, although the function of different lymphocyte subsets in the response to sepsis is unclear. γδ T cells are found largely in epithelial‐rich tissues, and previous studies of γδ T cells in models of sepsis have yielded divergent results. In the present study, we examined the function of γδ T cells during sepsis in mice using cecal ligation and puncture (CLP). Mice deficient in γδ T cells had decreased survival times and increased tissue damage after CLP compared with wild‐type mice. Furthermore, bacterial load was increased in γδ T cell‐deficient mice, yet antibiotic treatment did not change mortality. Additionally, we found that recruitment of neutrophils and myeloid suppressor cells to the site of infection was diminished in γδ T cell‐deficient mice. Finally, we found that circulating levels of IFN‐γ were increased, and systemic levels of IL‐10 were decreased in γδ T cell‐deficient mice after CLP compared with wild‐type mice. γδ T cell‐deficient mice also had increased intestinal permeability after CLP compared with wild‐type mice. Neutralization of IFN‐γ abrogated the increase in intestinal permeability in γδ T cell‐deficient mice. The intestines taken from γδ T cell‐deficient mice had decreased myeloperoxidase yet had increased tissue damage as compared with wild‐type mice. Collectively, our data suggest that γδ T cells modulate the response to sepsis and may be a potential therapeutic target. |
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