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Enhanced systemic antibacterial resistance was acquired by ACF1 (H-2ad) and B6D2F1 (H-2bd) mice bearing allogenetic BP-3 (H-2b) and SA-1 (H-2a) footpad tumors, respectively. This effect was dose dependent, in that the implantation of greater numbers of tumor cells produced larger tumors and higher levels of nonspecific resistance. Although the rejection of the tumor was T-cell dependent, the generation of nonspecific resistance was not. Thus, T-cell-deficient mice bearing progressively growing tumor allografts generated significant levels of antibacterial resistance. Two mechanisms were found to be involved in the generation of nonspecific resistance: (i) an acquired radioresistant mechanism responsible for initially destroying a large proportion of injected bacteria and (ii) an acquired radiosensitive mechanism responsible for destroying a significant number of bacteria after 24 h.

Generation of enhanced macrophage-mediated antibacterial resistance in animals responding to tumor allografts