Hypoxia enhances the effect of lipopolysaccharide-stimulated IL-1β expression in human periodontal ligament cells

被引:0
作者
Jittima Pumklin
Kanokporn Bhalang
Prasit Pavasant
机构
[1] Chulalongkorn University,Research Unit of Mineralized Tissue, Faculty of Dentistry
[2] Naresuan University,Department of Restorative Dentistry, Faculty of Dentistry
[3] Chulalongkorn University,Department of Oral Medicine, Faculty of Dentistry
[4] Chulalongkorn University,Department of Anatomy, Faculty of Dentistry
来源
Odontology | 2016年 / 104卷
关键词
Hypoxia; Interleukin-1beta; Human periodontal ligament cells; Lipopolysaccharide;
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中图分类号
学科分类号
摘要
Oral infection is inflammatory disease caused by bacteria. A major component of gram negative bacteria membrane associated with inflammation is lipopolysaccharide (LPS). Currently, evidence presenting the combined effect of LPS and hypoxia to inflammatory response in human periodontal ligament cells (HPDLs) was yet lacking. Here, we studied whether the influence of oxygen on LPS-stimulated inflammatory cytokines in HPDLs. HPDLs were stimulated with LPS in normoxia and hypoxia for 24 h. The mRNA and protein expression of inflammatory cytokines were examined by polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. The intracellular mechanisms of these effects were investigated by chemical inhibitors and small interfering RNA (siRNA). The results showed that LPS-stimulated IL-1β, IL-6, IL-8 in HPDLs in both hypoxia and normoxia. Hypoxia condition enhanced the effect of LPS-stimulated cytokines expression. Apigenin, the hypoxia-inducible factors (HIF)-1α inhibitor, totally prevented LPS-stimulated IL-1β expression in both normoxia and hypoxia. Similar to knockout HIF-1α gene expression by siRNA did \not prevent LPS-stimulated IL-1β expression. These data concluded that hypoxia increased virulence of LPS-stimulated IL-1β production in HPDLs.
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页码:338 / 346
页数:8
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共 149 条
[1]  
Akira S(2006)Pathogen recognition and innate immunity Cell 124 783-801
[2]  
Uematsu S(2012)Effect of resveratrol and modulation of cytokine production on human periodontal ligament cells Cytokine 60 197-204
[3]  
Takeuchi O(2009)Anti-inflammatory effects of apigenin on nicotine- and lipopolysaccharide-stimulated human periodontal ligament cells via heme oxygenase-1 Int Immunopharmacol 9 1374-1380
[4]  
Rizzo A(2012)Nicotine and lipopolysaccharide stimulate the production of MMPs and prostaglandin E2 by hypoxia-inducible factor-1alpha up-regulation in human periodontal ligament cells J Periodontal Res 47 719-728
[5]  
Bevilacqua N(1995)Inflammatory cytokine gene expression in human periodontal ligament fibroblasts stimulated with bacterial lipopolysaccharides Infect Immun 63 3576-3581
[6]  
Guida L(2012)Porphyromonas gingivalis-derived lipopolysaccharide-mediated activation of MAPK signaling regulates inflammatory response and differentiation in human periodontal ligament fibroblasts J Microbiol. 50 311-319
[7]  
Annunziata M(2014)Hypoxia augments lipopolysaccharide-induced cytokine expression in periodontal ligament cells Inflammation. 37 1413-1423
[8]  
Romano Carratelli C(2012)Differences in lipopolysaccharide- and lipoteichoic acid-induced cytokine/chemokine expression Intensive Care Med 38 324-332
[9]  
Paolillo R(2012)LPS-induced lung inflammation in marmoset monkeys—an acute model for anti-inflammatory drug testing PLoS One 7 e43709-9
[10]  
Jeong GS(2004)TLR signaling pathways Semin Immunol 16 3-444