Bioglass® attenuates a proinflammatory response in mouse peritoneal endotoxicosis
Bioglass is a bioactive, resorbable ceramic particle that was developed to assure binding to living tissues. Bioglass is currently employed to fill osseus defects in oral surgery, and it possesses both unique anti-inflammatory and antimicrobial properties. In an effort to determine whether Bioglass...
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Veröffentlicht in: | Shock (Augusta, Ga.) Ga.), 2002-02, Vol.17 (2), p.135-138 |
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Sprache: | eng |
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Zusammenfassung: | Bioglass is a bioactive, resorbable ceramic particle that was developed to assure binding to living tissues. Bioglass is currently employed to fill osseus defects in oral surgery, and it possesses both unique anti-inflammatory and antimicrobial properties. In an effort to determine whether Bioglass may be useful as an adjunct anti-inflammatory device in local inflammatory processes, we examined whether exposure of the peritoneal cavity to Bioglass would induce a pro- or anti-inflammatory response, and then modulate a subsequent proinflammatory response to endotoxin. Three- to fifty-milligram doses of 5 pm Bioglass were administered intraperitoneally in C57BL/6 mice. Total leukocyte, myeloperoxidase, and cytokine levels in the peritoneal wash fluid were determined. In addition, the peritoneal cavity was preexposed to Bioglass, and was then subjected to a subsequent endotoxin administration. All doses of Bioglass were found to induce a significant peritoneal IL-6 response; however, Bioglass did not induce a TNF-alpha, IL-1alpha, IL-10, or a white cell recruitment into the peritoneal lavage fluid. Pretreatment of the peritoneal cavity with Bioglass produced a transient reduction in the proinflammatory response to endotoxin. We conclude that exposure to Bioglass produces an IL-6 response without concurrent expression of TNF-alpha or IL-1alpha. Bioglass appears to transiently suppress the inflammatory response to endotoxin, possibly through the early induction of IL-6. These findings suggest that Bioglass may offer a unique approach in modifying the inflammatory response in local tissue compartments. |
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ISSN: | 1073-2322 1540-0514 |
DOI: | 10.1097/00024382-200202000-00009 |