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Radiation combined injury enhances iNOS expression and cytokine concentrations, delays wound closure, and alters ileal villi histology

Radiation combined injury (CI) results in mortality greater than that following radiation injury (RI) or skin‐wound trauma. The molecular mechanism for this increase is not clear. In this study, mice were given 9.75 Gy r‐radiation followed by a 15% total body skin surface wound. On 1d, 3d, and 7d after RI or CI, sections of ileum and skin were removed and histologically examined. Also, iNOS in ileum and skin and serum cytokines were determined. RI but not wounding vastly shortened and widened villi 3 d post‐RI, whereas CI resulted in smaller alterations in villus. However, the serosal layer was thinner after CI than after RI. The skin in CI mice was less cellular with a smaller healing bud than in wounded mice resulting in significantly delayed wound closure times after CI from about 14 d to 28 d. CI enhanced the levels of iNOS in both tissues that were upregulated by increases in transcriptional factors KLF6, NF‐kB, and NF‐IL6. The latter was related to a burst in cytokine concentrations including IL‐1b, ‐6, ‐8, ‐9, ‐10, ‐13, and c‐GSF. Bacteria were isolated from heart blood and liver, indicating translocation from intestinal tract and wound site may have induced increases in these cytokines. The data are consistent with the idea that increases in iNOS and cytokines by CI may contribute to the CI‐induced mortality. Agents that inhibit iNOS and the cytokine cascade may ameliorate CI‐induced sequelae including death.