2009年2月
Alendronate augments interleukin-1β release from macrophages infected with periodontal pathogenic bacteria through activation of caspase-1
Toxicology and Applied Pharmacology
- ,
- ,
- ,
- 巻
- 235
- 号
- 1
- 開始ページ
- 97
- 終了ページ
- 104
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1016/j.taap.2008.11.005
Nitrogen-containing bisphosphonates (NBPs) are anti-bone-resorptive drugs with inflammatory side effects that include osteomyelitis and osteonecrosis of the jaw. Oral bacteria have been considered to be a trigger for these NBP-associated jaw bone diseases. The present study examined the effects of alendronate (a typical NBP) and clodronate (a non-NBP) on the production of proinflammatory cytokines by macrophages infected with Porphyromonas gingivalis and Tannerella forsythia, which are important pathogens of periodontal diseases. Pretreatment with alendronate augmented IL-1β, but not TNFα, production by macrophages infected with P. gingivalis or T. forsythia. This augmentation of IL-1β production was inhibited by clodronate. Furthermore, caspase-1, a promoter of IL-1β production, was activated by treatment with alendronate, and caspase-1 inhibitor reduced the production of IL-1β induced by alendronate and P. gingivalis. These results suggest that NBPs augment periodontal pathogenic bacteria-induced IL-1β release via caspase-1 activation, and this phenomenon may contribute to the development of NBP-associated inflammatory side effects including jaw osteomyelitis. Co-treatment with clodronate may prevent and/or reduce these inflammatory effects induced by NBPs. © 2008 Elsevier Inc. All rights reserved.
- リンク情報
-
- DOI
- https://doi.org/10.1016/j.taap.2008.11.005
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/19063908
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000263541600012&DestApp=WOS_CPL
- URL
- https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=59249084288&origin=inward
- ID情報
-
- DOI : 10.1016/j.taap.2008.11.005
- ISSN : 0041-008X
- PubMed ID : 19063908
- SCOPUS ID : 59249084288
- Web of Science ID : WOS:000263541600012