Although strains of attenuated Salmonella typhimurium and wild-type Escherichia coli show similar tumor-targeting capacities, only S. typhimurium significantly suppresses tumor growth in mice. The aim of the present study was to examine bacteria-mediated immune responses by conducting comparative analyses of the cytokine profiles and immune cell populations within tumor tissues colonized by E. coli or attenuated Salmonellae. CT26 tumor-bearing mice were treated with two different bacterial strains: S. typhimurium defective in ppGpp synthesis (ΔppGpp Salmonellae) or wild-type E. coli MG1655. Cytokine profiles and immune cell populations in tumor tissue colonized by these two bacterial strains were examined at two time points based on the pattern of tumor growth after ΔppGpp Salmonellae treatment: 1) when tumor growth was suppressed ('suppression stage') and 2) when they began to re-grow ('re-growing stage'). The levels of IL-1β and TNF-α were markedly increased in tumors colonized by ΔppGpp Salmonellae. This increase was associated with tumor regression; the levels of both IL-1β and TNF-α returned to normal level when the tumors started to re-grow. To identify the immune cells primarily responsible for Salmonellae-mediated tumor suppression, we examined the major cell types that produce IL-1β and TNF-α. We found that macrophages and dendritic cells were the main producers of TNF-α and IL-1β. Inhibiting IL-1β production in Salmonellae-treated mice restored tumor growth, whereas tumor growth was suppressed for longer by local administration of recombinant IL-1β or TNF-α in conjunction with Salmonella therapy. These findings suggested that IL-1β and TNF-α play important roles in Salmonella-mediated cancer therapy. A better understanding of host immune responses in Salmonella therapy may increase the success of a given drug, particularly when various strategies are combined with bacteriotherapy.
The purpose of this study was to compare the effects of Korean mindfulness-based stress reduction (K-MBSR), walking, and patient education regarding diabetes mellitus (DM) on stress response, glycemic control, and vascular inflammation in patients with diabetes mellitus. A cluster randomized trial including 56 adults with diabetes mellitus (K-MBSR group = 21, walking group = 18, patient education group = 17) was conducted between 13 July and 14 September 2012. The questionnaire included the Diabetes Distress Scale and Perceived Stress Response Inventory. Fasting blood samples were used to measure levels of cortisol, blood glucose, plasminogen activator inhibitor-1 (PAI-1), and tissue plasminogen activator (t-PA). There were no statistically significant differences between the effects of K-MBSR, walking, and patient education on stress, glycemic control, or vascular inflammation. However, in the K-MBSR and walking groups, significant reductions in the levels of serum cortisol and PAI-1 were observed. A significant reduction in psychological responses to stress was observed in the walking and patient education groups. Longitudinal studies could provide better insight into the impact of K-MBSR, walking, and patient education on health outcomes in adults with diabetes mellitus.
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