Evidence-based products

Study Claim: Yeast-derived beta-glucan enhances the ability of certain human immune cells to navigate to the site of a bacterial infection.

Published: Tsikitis VL, et al. Beta-glucan affects leukocyte navigation in a complex chemotactic gradient. Surgery 2004 Aug; 136(2):384-9.

Abstract: Soluble beta-glucan binds to receptors (CR3) on neutrophils, the most abundant type of innate immune cell in the body, and benefits the host defence by increasing the killing capacity of the neutrophils, and by migration or chemotaxis to the site of an infection. Neutrophils are attracted to the site by blood proteins called chemoattractants and are among the first cells to respond to infection or injury.

Priming the neutrophils with beta-glucan increases their ability to sense complement fragments emanating from the site. As a result, beta-glucan helps neutrophils locate the bacterial mother lode within infected tissue. This more rapid response results in faster microbial clearance and healing.

In an experiment designed to measure cell migration, human neutrophils were placed in chambered slides with chemoattractants C5a or IL-8. Whereas both C5a and IL-8 are capable of attracting neutrophils, the former is formed and released at the site of a bacterial infection while the latter is released from patient tissue in the vicinity of the infectious focus. After leaving the bloodstream, neutrophils are challenged with the need to navigate through multiple attractive signals and give priority to those derived from bacteria in order to locate the infectious source. In this study, beta-glucan significantly improves the ability of neutrophils to interpret these signals by increasing their sensitivity to C5a and blunting their movement to IL-8. Taken together, this results in an improved navigational compass leading cells directly to the bacterial source.

Potential applications: for use in pharmaceuticals, nutritional supplements, functional foods, cosmetics, and animal feed and nutrition.

More info:
+1 651 675 0300

Study claim: SierraSil, alone, and in combination with an extract of cat?s claw, Vincaria, limits human cartilage degradation-activated chondrocytes.

Published: Miller M, et al. Suppression of human cartilage degradation and chondrocyte activation by a unique mineral supplement (SierraSil) and a cat?s claw extract, Vincaria. J Am Nutraceutic Assoc 2004; 7(2):22-9.

Abstract: Cartilage degradation contributes to the dysmobility, pain and compromised quality of life associated with rheumatoid arthritis and osteoarthritis. SierraSil was subjected to neutral, alkali and acid washes, followed by neutralisation before addition to cartilage explants or cultured chondrocytes (0.05, 0.1 and 0.2 mcg/ml). Vincaria, an alkaloid-depleted aqueous extract of cat?s claw (Uncaria guianensis), was studied in combination with SierraSil (final concentrations of 2.5, 5 and 10ng/ml). Chondrocytes were activated with the addition of the inflammatory cytokine interleukin-1beta. Measured outcomes were media nitrate, nitrite levels as an index of nitric oxide production and media glycosaminoglycan (GAG) concentrations as an index of matrix breakdown.

Following neutral or alkali washes, SierraSil was ineffective in reducing nitric oxide release, although a small reduction in GAG release was observed with neutral extracts. However, the combination of SierraSil plus Vincaria significantly reduced both GAG and nitric oxide release. Following an acid wash to mimic passage through the stomach, SierraSil significantly reduced IL-1beta-induced GAG release by 68-73 per cent, and SierraSil plus Vincaria by 58-77 per cent. Production of NO by chondrocytes was also reduced by acid-washed SierraSil alone and was more pronounced with the SierraSil/Vincaria combo.

Attenuation of these events suggests that this herb-mineral combination limits cartilage destruction by curtailing these transcriptional events in chondrocytes.

Potential applications: This dietary supplement may limit joint destruction and dysmobility associated with arthritis.

More info:
+1 888 888 1464

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