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Epidermal tumors belong to the most frequent type of neoplasms, and tumor-associated accumulation of mast cells (MCs) has first been observed more than a century ago. Therefore, MCs have been implicated in tumor development and growth; however, the results regarding the role of MC in cutaneous de novo carcinogenesis are still controversially discussed. Here, we subjected MC-deficient Kit(W) /Kit(W-v) mice to chemical skin carcinogenesis. Tumors were induced using the carcinogen 7,12-dimethylbenz[a]-anthracene and subsequent treatment with the tumor promoter 12-tetradecanoyl-phorbol-13-acetat. The treatment resulted in pronounced inflammatory cell infiltrates that were diminished in MC-deficient animals. Unexpectedly, tumor development and growth was significantly increased in MC-deficient Kit(W) /Kit(W-v) mice. The repair of their MC deficiency by local adoptive transfer of MCs normalized tumor incidence and growth. The recruitment of skin-infiltrating immune cells, particularly of F4/80+ monocytes, Gr-1+ granulocytes, B220+ B cells and CD8+ T lymphocytes, to sites of tumor development was, in part, also controlled by MCs. Recent evidence indicated the importance of local antitumor tissue immunity which prevents tumor development. These findings suggest a critical role for MCs in mediating these host antitumor immune responses in the skin., (© 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Background: The mast cell's (MC) ability to rapidly release presynthesized mediators allows it to play a critical role in the immune system's first-line response to pathogens. Although recent research has illuminated the role of MCs in bacterial infection, little is known about how non-pathogenic bacteria influence MC responses., Objective: To characterize the influence of non-pathogenic Escherichia coli bacteria on MCs., Results: High concentrations of live E. coli strongly down-modulated the degranulation of murine peritoneal MCs under all activator conditions. Bacteria did not induce MC degranulation by themselves, and staining of MCs showed they were still entirely viable. Dead bacteria and bacterial supernatant had no effect on MC degranulation. Ex vivo experiments confirmed that E. coli exposure down-modulates subsequently induced MC degranulation and that this effect lasts for up to a few days after exposure., Conclusion: Our results show that high doses of non-pathogenic E. coli bacteria can function as a strong, direct inhibitor of MC degranulation. This suggests a possible basis for future antiallergic treatment or prophylaxis with commensal bacteria, i.e. probiotics.