Submitted to: Biological Trace Element Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 28, 2009
Publication Date: June 1, 2010
Repository URL: http://handle.nal.usda.gov/10113/42487
Citation: Nielsen, F.H. 2010. Silicon Deprivation Does Not Significantly Modify the Acute White Blood Cell Response but Does Modify Tissue Mineral Distribution Response to an Endotoxin Challenge. Biological Trace Element Research. 135:45-55. Interpretive Summary: Silicon has been long suspected to be a beneficial bioactive, if not essential, element for higher animals and humans. Some studies have indicated that silicon helps in the immune response; that is, promotes the production (chronic response) of some white blood cells and other cell molecules (cytokines) that attack an invading material such as bacteria that cause illness. An experiment was performed to determine whether silicon status also affects the immediate movement of cells and their cytokine production in the body, which is called the acute phase inflammatory response, when injected with a bacterial cell component (lipopolysaccharide, LPS) that induces such a response. Weanling female rats were fed for seven weeks a diet that contained either 1.9 micrograms (silicon-deprived) of silicon per kilogram, or the same diet supplemented with 35 micrograms of silicon per kilogram. Two hours after injection of LPS, inflammatory white blood cells that fight bacterial infection (lymphocytes, monocytes, eosinophils, and basophils) were markedly reduced in blood because of movement into tissues to attack LPS. The inflammatory cytokines tumor necrosis factor alpha and osteopontin, which are involved in fighting infection, were increased in blood. Silicon deprivation did not significantly affect any of these responses to LPS. These findings indicate that silicon deprivation does not affect the acute-phase response of decreased circulating white blood cells and increased inflammatory cytokines induced by LPS injection. However, silicon in liver, and silicon, iron, and zinc in femur were increased by LPS injection only in silicon-deprived rats. Silicon deprivation also increased one white blood cell (monocyte) and blood osteopontin, and decreased femur zinc in rats not injected with LPS. Changes in tissue iron and zinc occur in the inflammatory response. These responses to silicon deprivation support previous reports suggesting that silicon is beneficial through promoting inflammatory cell production in the chronic-phase inflammatory response.
Technical Abstract: An experiment with rats was conducted to determine whether silicon deprivation affects the acute-phase immune response to an endotoxin challenge. Weanling female rats were assigned to two weight-matched groups of 24; one group was fed a basal diet containing about 1.9 µg Si/kg, the other group was fed the basal diet supplemented with 35 µg Si/kg as arginine silicate inositol complex. After being fed their respective diets for eight weeks 12 rats in each group were injected subcutaneously with 1 mg lipopolysaccharide (LPS)/kg body weight, the other 12 rats in each group were injected with deionized water. Two hours after injection the rats were anesthetized with ether for collection of blood (for plasma), liver and femurs, and then euthanized by decapitation. LPS injection decreased total white blood cell, lymphocyte, monocyte, eosinophil, and basophil counts by 80%-90%, but did not affect neutrophil counts. LPS injection also increased plasma tumor necrosis factor-a and osteopontin and decreased plasma hyaluronic acid. Silicon deprivation did not significantly affect any of these responses to LPS. Silicon in liver, and silicon, iron and zinc in femur were increased by LPS injection only in silicon-deprived rats. Silicon deprivation also increased monocyte counts and osteopontin, and decreased femur zinc in rats not injected with LPS. The findings indicate that silicon deprivation does not affect the acute-immune phase decrease in inflammatory cell numbers and increase in inflammatory cytokines in response to an endotoxin challenge. Silicon deprivation, however, apparently causes slight chronic inflammation and might influence inflammatory cell proliferation in the chronic-phase inflammatory response.