Leah M Pyter1, Daniel B McKim2, Yasmin Husain3, Humberto Calero3, Jonathan P Godbout4, John F Sheridan5, Phillip T Marucha3, Christopher G Engeland3. 1. Institute for Behavioral Medicine Research, Ohio State University Wexner Medical Center, Columbus, Ohio; Departments of Psychiatry and Behavioral Health, Ohio State University, Columbus, Ohio; Department of Neuroscience, Ohio State University, Columbus, Ohio; Center for Wound Healing and Tissue Regeneration, College of Dentistry, University of Illinois at Chicago, Chicago, Illinois. Electronic address: leah.pyter@osumc.edu. 2. Institute for Behavioral Medicine Research, Ohio State University Wexner Medical Center, Columbus, Ohio. 3. Center for Wound Healing and Tissue Regeneration, College of Dentistry, University of Illinois at Chicago, Chicago, Illinois. 4. Institute for Behavioral Medicine Research, Ohio State University Wexner Medical Center, Columbus, Ohio; Department of Neuroscience, Ohio State University, Columbus, Ohio. 5. Institute for Behavioral Medicine Research, Ohio State University Wexner Medical Center, Columbus, Ohio; Department of Biosciences, College of Dentistry, Ohio State University, Columbus, Ohio.
Abstract
BACKGROUND: Before primary oral tumors are treated, various prophylactic procedures that require tissue repair are often necessary (e.g. biopsies, tooth extractions, radiation, and tracheotomies). Wound healing and tumor growth harness similar immune/inflammatory mechanisms. Our previous work indicates that tumors impair wound healing, although the extent to which tissue repair conversely influences tumor growth is poorly understood. Here, we test the hypothesis that dermal wound healing exacerbates primary tumor growth and influences tumor immunobiology. MATERIALS AND METHODS: Female, immunocompetent mice were inoculated subcutaneously with murine oral cancer cells (AT-84) to induce flank tumors. Half of the mice received dermal excisional wounds (4 × 3.5 mm diameter) on their dorsum 16 days later, whereas the skin of controls remained intact. Tumor and blood tissues were harvested 1 and 5 days post wounding, and tumor myeloid cell populations and inflammatory gene expression were measured. Circulating myeloid cells, cytokines, and corticosterone were also quantified. RESULTS: Wounding increased tumor mass, early tumor infiltration of macrophages, and tumor inflammatory gene expression. While wounding attenuated tumor growth-induced increases in circulating myeloid cells, no effects of wounding on circulating cytokine/endocrine measures were observed. CONCLUSIONS: These results indicate that modest skin immune/inflammatory processes can enhance distal tumor growth and alter innate tumor immunity. The implication for this work is that, in the presence of a tumor, the benefits of tissue-damaging procedures that occur clinically must be weighed against the potential consequences for tumor biology.
BACKGROUND: Before primary oral tumors are treated, various prophylactic procedures that require tissue repair are often necessary (e.g. biopsies, tooth extractions, radiation, and tracheotomies). Wound healing and tumor growth harness similar immune/inflammatory mechanisms. Our previous work indicates that tumors impair wound healing, although the extent to which tissue repair conversely influences tumor growth is poorly understood. Here, we test the hypothesis that dermal wound healing exacerbates primary tumor growth and influences tumor immunobiology. MATERIALS AND METHODS: Female, immunocompetent mice were inoculated subcutaneously with murineoral cancer cells (AT-84) to induce flank tumors. Half of the mice received dermal excisional wounds (4 × 3.5 mm diameter) on their dorsum 16 days later, whereas the skin of controls remained intact. Tumor and blood tissues were harvested 1 and 5 days post wounding, and tumor myeloid cell populations and inflammatory gene expression were measured. Circulating myeloid cells, cytokines, and corticosterone were also quantified. RESULTS: Wounding increased tumor mass, early tumor infiltration of macrophages, and tumor inflammatory gene expression. While wounding attenuated tumor growth-induced increases in circulating myeloid cells, no effects of wounding on circulating cytokine/endocrine measures were observed. CONCLUSIONS: These results indicate that modest skin immune/inflammatory processes can enhance distal tumor growth and alter innate tumor immunity. The implication for this work is that, in the presence of a tumor, the benefits of tissue-damaging procedures that occur clinically must be weighed against the potential consequences for tumor biology.
Authors: Kyle A Sullivan; Savannah R Bever; Daniel B McKim; Jonathan P Godbout; John F Sheridan; Karl Obrietan; Leah M Pyter Journal: Brain Behav Immun Date: 2019-05-17 Impact factor: 7.217