Background
In vitro and in vivo studies demonstrate that nutritional supplementation reduces inflammation and inflammatory markers associated with T-cell adhesion mechanisms. Here, we investigate the effects of the nutritional supplements, Natramune (PDS-2865) and PureWay-C, on xenobiotic-induced alpha5beta1 integrin-mediated T-cell adhesion to fibronectin.
Material and Method
The human CD4+ lymphoblastoid cell line CEM SS was treated with combinations of bifenthrin, blocking antibodies to human beta1 and alpha5 integrin, and nutrient supplements. After 30 minutes unattached cells were aspirated and the percent of attached cells was determined.
Results
Bifenthrin stimulated T-cell adhesion to fibronectin at concentrations between 1.0 and 100 microM with a maximal stimulation of 8.3-fold at 10 microM. At 500 microg/ml, Natramune reduced 100 microM bifenthrin-induced adhesion by nearly 90%. PureWay-C reduced by 1.5-fold the level of T-cell adhesion stimulated by bifenthrin concentrations of both 10 microM and 100 microM. The combination of Natramune and PureWay-C resulted in a 6.3 and 7.5-fold inhibition at 10 microM and 100 microM bifenthrin respectively. Antibody blocking studies demonstrated that bifenthrin induced CEM SS adhesion to fibronectin is mediated through alpha5beta1 integrin. Inhibition of T-cell adhesion achieved by anti-integrin antibodies was further reduced with 50 and 500 microg/ml Natramune treatment. Pretreatment of fibronectin with Natramune did not alter induced T-cell adhesion to fibronectin.
Conclusions
These data demonstrate that xenobiotic-induced alpha5beta1 integrin mediated T-cell adhesion to fibronectin is reduced by nutritional supplementation with Natramune (PDS-2865) and PureWay-C. These data suggest the possibility that inflammatory responses associated with exposure to pollutants can be mitigated by nutritional supplementation.

Keywords: Pyrethrins - pharmacology, Xenobiotics - pharmacology, Integrin alpha5beta1 - physiology, Fibronectins - metabolism, Dietary Supplements, Cell Adhesion - physiology, CD4-Positive T-Lymphocytes - drug effects