Blood-borne bacteria, fungi and viral agents can activate cells of the innate immune system by interacting with pattern-recognition or Toll receptors on the surface of immune cells. We demonstrate here that mRNA for Toll receptors is ubiquitously expressed in a range of transformed and normal cell types. These findings raise the possibility that infection could induce an inflammatory response in somatic tissues and this might i), provide a milieu for changes in normal cells that lead to neoplastic growth and/or ii), that it might provide conditions suitable for enhancing the growth of an existing neoplastic lesion. As a preliminary step to investigate this, we have studied the response of breast tumour MCF-7 cells to a sonicate of a mixed bacteria cell population. Using quantitative PCR (QPCR) and primers for Toll receptors 1 to 10, we have shown that 24 h exposure to the bacterial cell sonicate up-regulates the expression of mRNA for Toll-2 and Toll-4 by between 5 and 8 fold. The expression of other Toll receptors was not significantly altered. Given that the cytokine IL6 is induced in immune cells by ligands of Toll receptor 4, we have further demonstrated by QPCR, that mRNA for this inflammatory cytokine is markedly induced in MCF-7 cells by exposure to the sonicated bacteria and that this effect is blocked by prior exposure of the MCF-7 cells to dexamethasone. These finding strongly suggest that the full Toll-mediated inflammatory system is present in breast tumour cells and they provide a rationale for tumour therapy, targeted to the Toll receptors.