Probiotics and tumour growth

Several studies in animal models have investigated the effects of probiotic administration on immune responses and tumour regression. Initial studies had indicated that systemically delivered LAB cells could potentiate ex vivo leucocyte tumoricidal and lymphoproliferative responses and could limit the growth of both primary and secondary tumours at several tissue sites in vivo (Kato et al., 1981, 1983). More recent studies have focused on the use of orally delivered probiotics and anti-tumour immunity. L. casei Shirota has received a great deal of research attention. Orally delivered L. casei Shirota was shown to reduce the establishment and growth of inoculated syngeneic sarcoma cells in BALB/c mice, concomitant with an increased lymphoproliferative response and capacity to secrete the cytokine IL-2 by splenic T-cells in these animals (Yokokura, 1994). Furthermore, growth of secondary tumours was inhibited in probiotic-fed mice following tumour resection, again linked to enhanced lymphocyte responsiveness (Kato et al., 1994). Lactobacillus plantarum (strain L-137) has also been shown to retard the growth of implanted P3881D tumour cells in syngeneic DBA/2 mice, and in this case the mechanism was suggested to be a systemic elevation of the pro-cellular-immunity cytokine IL-12, favouring anti-tumour cellular immune responses (Murosaki et al., 2000).

Additional studies on L. casei Shirota have indicated that this strain may also have anti-carcinogenic effects related to enhanced immune activity. Takagi et al. (1999) have recently demonstrated that mice fed the probiotic developed fewer systemic tumours following injection of the hydrocarbon carcinogen 3-methylcholanthrene and that lymphoproliferative responses and the IL-2-secreting activity of splenic T-cells were retained, while the comparative immune responses in non-probiotic-fed mice declined markedly during tumour development. In similar studies, probiotic-containing yoghurt has been shown to limit intestinal-tract tumour development in mice injected with the carcinogen 1,2-dimethylhydrazine (Perdigon et al., 1998), and this reduction was associated with enhanced infiltrations of CD4+ T lymphocytes into the intestinal tissues in these mice. Other strains of Lactobacillus have also been shown to limit the incidence and mean developmental size of colonic adenocarcinomas in Sprague-Dawley rats fed 1,2-dimethylhydrazine (Balansky et al., 1999; Mcintosh et al. 1999), although associated immune responses were not investigated in these studies. A further anti-cancer mechanism of probiotics involves the deconjugation of potentially mutagenic enzymes in the gut lumen, although this mechanism is not thought to have an immune component.

No longitudinal clinical trials have yet been undertaken to determine the potentially protective effects of immunoactive probiotics in the reduction of tumour incidence/development. However, a few studies have investigated the ability of probiotic LAB strains to retard tumour growth in cancer patients. L. casei Shirota was shown to reduce the recurrence of superficial bladder cancer in adult patients following resection (Aso et al., 1995) and also to delay the onset of tumour recurrence (Aso et al., 1992; Table 13.2). Although associated cellular immune parameters were not reported in these studies, work in adult colon-cancer patients has shown that oral L. casei Shirota delivery can enhance circulating NK-cell activity (Sawamura et al., 1994), suggesting that tumour limitation may be the result of enhanced immunoactivity imparted by the probiotic. In contrast, however, a recent study has reported that L. casei Shirota does not enhance NK-cell tumoricidal activity in healthy adult subjects (Spanhaak et al., 1998).

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