THERMAL INJURY ELEVATES THE INFLAMMATORY MONOCYTE SUBPOPULATION IN MULTIPLE COMPARTMENTS
Monocyte
DOI:
10.1097/shk.0b013e31805362ed
Publication Date:
2007-07-06T08:21:34Z
AUTHORS (9)
ABSTRACT
Recent publications have demonstrated that human resident and inflammatory monocyte (IM) subpopulations equivalents in rodents. The effect of thermal injury upon these has not been studied. Mice were given a scald burn killed on postburn days (PBDs) 2, 4, 8. Bone marrow, blood, spleen white cells isolated, the percentage monocytes (CD11b LY6C), IMs progenitors (macrophage-colony-forming unit [M-CFU]) determined. ability each population to make TNF-alpha was determined by intracellular cytokine staining. Finally, sorted fractions from PBD 8 inhibit lymphocyte proliferation performed. We noted there an increase M-CFU blood at 8, but marrow only had nonsignificant M-CFU. All compartments showed significant number no changes seen. In all compartments, major source TNF-alpha. accompanied chemokine chemoattractant protein 1 constitutively high levels progenitor stromal-derived factor 1alpha. After injury, mice deficient receptor for soluble equal splenic monocytes, as did wild-type mice, suggesting this is essential effect. conclude model, are vivo
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