Abstract

Objective: Thermal injury induces inflammatory monocyte/macrophages in multiple tissues. Blood monocytes are the precursors of these cells, and consist of two populations. The CD11b+ LY6C dim population ("normal monocyte") enters noninflamed tissue in the steady state under the influence of fractalkaline. The CD11b+ LY6C bright population ("inflammatory monocyte") enters inflamed tissue under the influence of MCP-1. The effect of thermal injury upon these subpopulations is not known. Methods: Mice were given a 25% full thickness burn, and spleens or heparinzed whole blood was drawn at post burn days 2, 4 and 8. Cells were stained with FITC LY6C and APC labeled CD11b. The cells fixed with paraformaldehyde, and analyzed by flow cytometry. Results: There was a progressive increase in inflammatory monocytes in the blood from post burn day 4 onwards (see Figure). In contrast, there was no change in the percentage of normal monocytes in the blood at any post burn time. At post burn days 4 and 8, the spleen contained significantly increased numbers of inflammatory monocytes relative to controls. These changes correlated with a significantly increased splenic expression of MCP-1 at post burn day 2. Conclusion: The increase in blood CD11b+ LY6G++ monocytes after thermal injury is a possible mechanism for the entrance of inflammatory cells into tissues after thermal injury.

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