Accelerated alveolar bone loss in mice lacking interleukin-10

被引:73
作者
Al-Rasheed, A
Scheerens, H
Rennick, DM
Fletcher, HM
Tatakis, DN
机构
[1] Ohio State Univ, Coll Dent, Sect Periodontol, Columbus, OH 43218 USA
[2] Loma Linda Univ, Sch Med, Div Microbial & Mol Genet, Loma Linda, CA USA
[3] DNAX Res Inst Mol & Cellular Biol Inc, Dept Immunol, Palo Alto, CA 94304 USA
[4] King Saud Univ, Coll Dent, Dept Prevent Dent Sci, Periodont Div, Riyadh, Saudi Arabia
[5] Loma Linda Univ, Sch Dent, Dept Periodont, Loma Linda, CA 92350 USA
关键词
alveolar bone loss; antibodies; disease models; interleukin-10; mice; knockout;
D O I
10.1177/154405910308200812
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Interleukin-10 regulates pro-inflammatory cytokines, including those implicated in alveolar bone resorption. We hypothesized that lack of interleukin-10 leads to increased alveolar bone resorption. Male interleukin-10(-/-) mice, on 129/SvEv and C57BL/6J background, were compared with age-, sex-, and strain-matched interleukin-10(+/+) controls for alveolar bone loss. Immunoblotting was used for analysis of serum reactivity against bacteria associated with colitis and periodontitis. Interleukin-10(-/-) mice had significantly greater alveolar bone loss than interleukin-10(+/+) mice (p = 0.006). The 30-40% greater alveolar bone loss in interleukin-10(-/-) mice was evident in both strains, with C57BL/6J interleukin-10(-/-) mice exhibiting the most bone loss. Immunoblotting revealed distinct interleukin-10(-/-) serum reactivity against Bacteroides vulgatus, B. fragilis, Prevotella intermedia, and, to a lesser extent, against B. forsythus. The results of the present study suggest that lack of interleukin-10 leads to accelerated alveolar bone loss.
引用
收藏
页码:632 / 635
页数:4
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