Some members of the microbiota have been shown to be effective strategies for inhibiting tumor growth through stimulation of host anti-tumor immune responses. Anti-tumor immune effects were observed when Lactobacillus plantarum (Lp), a member of the gut microbiota, was used to treat colorectal cancer in mice. Moreover, constituents of bacteria, including peptidoglycan (PG), have been shown to exhibit tumoricidal effects. The aim of this study was to investigate the anti-tumor effects of Lp on serum levels of angiogenic and immunostimulatory cytokines in melanoma-bearing mice in vivo; as well as the effect of PG on the growth of mouse melanoma and breast cancer cells in vitro. Fifty C57BL/6 female mice were divided into two groups. Prior to tumor implantation, Lp was administered via oral gavage for 2 weeks to the experimental group. After receiving subcutaneous injections of B16F10 melanoma cells, Lp administration was continued once per week for 3 weeks to the experimental group. After the last bacterial administration, serum levels of Vascular Endothelial Growth Factor (VEGF) and Interleukin-12 (IL-12) were determined by ELISA. Additionally, mice from both groups were monitored for survival. Moreover, B16F10 melanoma and EMT6 breast cancer cells were incubated separately with two PG concentrations for 48 h and percent viability was determined. A significant decrease in the serum levels of VEGF and a significant increase in the serum levels of IL-12 were observed in the group treated with Lp Moreover, 20% survival rate was noted in the group treated with Lp In vitro, a marked decrease in the viability of mouse melanoma and breast cancer cells was observed 48 h post-incubation with PG. It appears that Lp possesses anti-tumor activity, by both stimulating the immune system and suppressing angiogenesis. Moreover, Lp appears to have a direct tumoricidal effect through PG.

Earlier reports indicated that Bovine Cartilage (BC) had antitumor effects but only a few in vitro and in vivo investigations were conducted to assess its mechanism of action. The aim of this study was to investigate some of the proposed mechanisms of action of BC on mouse melanoma cells both in vitro and in vivo and to determine if its effect on tumor cells is selective. One hundred and ten mice were divided into 5 groups and received Intraperitoneal (IP) injections of melanoma cells followed by treatment with BC using different routes of administration. Following a daily treatment period of 16 days, serum levels of VEGF and IL-12 were determined by ELISA at 2, 4 and 6 h after the last treatment dose. Additionally, 10 mice from each group were monitored for survival for 20 days post-last treatment. Moreover, melanoma and mouse mononuclear cells were incubated separately with increasing BC concentrations for 48 h and percent viability was determined. A significant decrease in the serum levels of VEGF and significant increase in the serum levels of IL-12 were observed in the groups treated with BC. Moreover 20% survival rate was noted in the group treated with BC both orally and IP, whereas 10% survival was noted in the groups given BC either IP or orally. In vitro, total eradication of melanoma cells was observed with 1000 µg mL −1 of BC. BC was not toxic to mouse mononuclear cells. The in vivo anti-tumor effect of BC was best observed when combined IP and oral doses were given and it appears that two of its actions are by activating macrophages as indicated by increases in IL-12 levels and blocking angiogenesis as indicated by decreases in VEGF levels. Finally BC showed selective toxicity against melanoma cells.

Ciprofloxacin seems to exhibit antitumor activity both in-vivo and in-vitro. This effect might be explained by several mechanisms such as directly inducing cancer cell death or altering the immune response through the modification of the normal microbiota.

Multiple sclerosis (MS) is an autoimmune demyelinating disorder of the central nervous system. We have previously demonstrated that an HHV-6 infection increases the risk of MS and that particular single nucleotide polymorphisms (SNPs) in the IL2RA and IL7RA genes modestly enhance the risk of this disease in HHV-6 positive subjects. To assess whether human leukocyte antigen (HLA) genetic determinants affect the risk of susceptibility to MS, blood samples were collected from 41 MS patients and 38 controls. Subject HLA genetic profiles were then determined by DNA sequence specific primers (SSP) typing. Detection of HHV-6 DNA was carried out using nested PCR while IL2RA and IL7RA allele detection was performed using restriction fragment length polymorphism (RFLP) analysis. We observed an increase in the risk of susceptibility to MS in individuals harboring the A*2301 (p=0.033) and the A*0301 (p=0.032) HLA alleles. Double positivity for the DQB1*0501 allele and HHV-6 enhanced the risk of this disease (p=0.036) while DQB1*0501 positivity by itself was not associated with the disorder. Combinational positivity for the IL2RA and IL7RA SNPs, HHV-6 in addition to the various HLA alleles did not result in significant MS risk increases in our study population. Hence, particular genetic determinants increase the risk of MS in HHV-6 positive subjects. These determinants do not exert the same effects in uninfected individuals.