Up-regulation of human immune system function by Donkey's Milk

Donkey's milk represents a good alternative to human milk because of its chemical characteristics similar to those of human's. In present study, the pro- and anti-inflammatory effects of donkey's milk were evaluated on peripheral blood mononuclear cells (PBMCs). PBMCs were isolated from 12 young and 12 aged normal subjects. PBMCs were cultured with or without the optimal and non-cytotoxic dose of pasteurized donkey's milk, and polymyxin B was used to inhibit the possible endotoxin contamination. Following 18 hours incubation, culture supernatants were harvested to measure the secreted Tumor necrosis factor-α (TNF-α), Interleukin-6 (IL-6), Interleukin-8 (IL-8) and Interleukin-10 (IL-10) by ELISA. Donkey's milk significantly increased TNF-α (p= 0.01), IL-8 (p< 0.0001), IL-6 (p< 0.0001) and IL-10 (p= 0.01) levels in PBMCs. In addition, the levels of IL-6 (p= 0.002), IL-8 (p= 0.002) and TNF-α (p= 0.002) from aged subjects were significantly higher compared with young subjects. In contrast with these data, the level of IL-10 was markedly reduced from aged subjects (p= 0.02). Considering the immune-potentiation effects of donkey's milk, it is suggested investigating milk as a beneficial dietary component for up-regulating the immune response in aged people

Possible potentiation of toxins from Prevotella intermedia, Prevotella nigrescens, and Porphyromonas gingivalis by cotinine.

BACKGROUND: Smoking is a recognized risk factor for the initiation and progression of periodontitis. However, the mechanism by which smoking induces its negative effects on the periodontium is not clear. This study aimed to test the hypothesis that synergy may occur between cotinine and bacterial products isolated from 3 putative periodontopathogens. METHODS: A chick embryo toxin assay was used to investigate bacterial toxins (cell-free extracellular toxins and cell-free cell lysates) from 5 species with and without cotinine. A total of 9 putative periodontopathogens (3 species) and 2 non-oral controls (2 species) were studied. The periodontal species were: Prevotella intermedia (n = 4), Prevotella nigrescens (n = 4), and Porphyromonas gingivalis (n = 1). The control species tested were: Staphylococcus aureus (n = 1) and Escherichia coli (n = 1). RESULTS: The toxicity kill was significantly greater than expected by simple addition alone (P <0.05, Fisher's exact test) between cotinine (800 ng/ml) and 1) the cell-free extracellular toxins of P. nigrescens MH1 and 2) the cell-free cell lysates of P. intermedia MH2. Synergy occurred with cotinine plus the cell-free extracellular toxins in all but 3 periodontal isolates, and the cell-free cell lysates in all but 2 periodontal isolates. Cotinine significantly (P <0.05, Fisher's exact test) enhanced the effects of cell-free extracellular toxins and cell lysates from one control species (E. coli), but not the other (S. aureus). CONCLUSIONS: These findings indicate that synergy in an in vitro assay can occur between cotinine and toxins from putative periodontopathogens. This may be one important mechanism by which smoking increases the severity of periodontitis.