The Potential of Honey as a Prebiotic Food to Re-engineer the Gut Microbiome Toward a Healthy State

Honey has a long history of use for the treatment of digestive ailments. Certain honey types have well-established bioactive properties including antibacterial and anti-inflammatory activities. In addition, honey contains non-digestible carbohydrates in the form of oligosaccharides, and there is increasing evidence from in vitro, animal, and pilot human studies that some kinds of honey have prebiotic activity. Prebiotics are foods or compounds, such as non-digestible carbohydrates, that are used to promote specific, favorable changes in the composition and function of the gut microbiota. The gut microbiota plays a critical role in human health and well-being, with disturbances to the balance of these organisms linked to gut inflammation and the development and progression of numerous conditions, such as colon cancer, irritable bowel syndrome, obesity, and mental health issues. Consequently, there is increasing interest in manipulating the gut microbiota to a more favorable balance as a way of improving health by dietary means. Current research suggests that certain kinds of honey can reduce the presence of infection-causing bacteria in the gut including Salmonella, Escherichia coli, and Clostridiodes difficile, while simultaneously stimulating the growth of potentially beneficial species, such as Lactobacillus and Bifidobacteria. In this paper, we review the current and growing evidence that shows the prebiotic potential of honey to promote healthy gut function, regulate the microbial communities in the gut, and reduce infection and inflammation. We outline gaps in knowledge and explore the potential of honey as a viable option to promote or re-engineer a healthy gut microbiome

Tumor Growth, Weight Loss, and Cytokines in SCID Mice

It has been proposed that immunoregulatory cytokines play a role in the onset and development of cancer cachexia, although evidence supporting this theory remains inconclusive. In the present study, SCID mice were implanted with one of two tumor cell lines known to induce weight loss in rats. Growth of the Morris 7777 hepatoma was associated with weight loss as well as increased levels of tumor necrosis factor and interleukins 1 and 6 in spleen cells of tumor-bearing mice. Growth of the MCA sarcoma did not induce weight loss, nor did it increase cytokine expression in spleen cells of tumor-bearing mice. We conclude that increased cytokine expression is associated with weight loss in tumor-bearing SCID mice, and immune activation for cytokine expression does not require the presence of T or B cells

Antigenicity of Human Melanoma Cells Transfected to Express the B7-1 Co-Stimulatory Molecule (CD80) Varies with the Level of B7-1 Expression

The aim of this study was to compare the antigenicity of human melanoma cells molecularly modified by particle-mediated gene transfer to have transient or stable expression of the B7-1 co-stimulatory molecule (CD80). The unmodified melanoma cells (mel5, m21) had no constitutive expression of B7-1, but 22%–28% of cells had transient B7-1 expression 24 h following transfection with cDNA for B7-1 (mel5-B7, m21-B7). In addition, 85%–90% of cells had stable B7-1 expression following transfection with cDNA for B7-1 and in vitro culture under selection conditions (mel5-B7neo, m21-B7neo). Allogeneic HLA-unmatched normal donor peripheral blood mononuclear cells (PBMC) secreted greater amounts of granulocyte/macrophage-colony-stimulating factor (GM-CSF) when incubated for 3 days with m21-B7neo than did PBMC incubated with m21-B7, which, in turn, secreted greater amount of GM-CSF than PBMC incubated with m21. Similarly, cell-mediated cytotoxicity against unmodified melanoma cells by PBMC co-cultured for 5 days with the modified or unmodified melanoma cells was proportional to the level of B7-1 expression on the stimulating cells. This cytolytic activity had both an HLA-class-I-restricted and an HLA-class-I-unrestricted component. Following 5 days of co-culture, PBMC expression of CD28, the ligand for B7-1, was down-regulated in proportion to the level of B7-1 expression on the stimulating melanoma cells. Thus, particle-mediated gene delivery of cDNA for B7-1 into human melanoma cells increased expression of functional B7-1 and enhanced the antigenicity of the gene-modified cells in proportion to their level of B7-1 expression