The Lipopolysaccharide from Porphyromonas gingivalis Induces Vascular Permeability.
- Author:
Su Ryun KIM
1
;
Seong Kyoon JEONG
;
Woo Sik KIM
;
Hwa Jin JEON
;
Hyun Joo PARK
;
Mi Kyoung KIM
;
Hye Ock JANG
;
Il YUN
;
Soo Kyung BAE
;
Moon Kyoung BAE
Author Information
1. Department of Oral Physiology, School of Dentistry, Pusan National University, Yangsan 626-870, Korea. mkbae@pusan.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
human vascular endothelial cells;
interleukin-8;
Porphyromonas gingivalis lipopolysaccharide;
vascular permeability
- MeSH:
Capillary Permeability;
Endothelial Cells;
Inflammation;
Interleukin-8;
Periodontal Diseases;
Porphyromonas;
Porphyromonas gingivalis;
RNA, Messenger
- From:International Journal of Oral Biology
2011;36(1):23-29
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Porphyromonas gingivalis, one of the major periodontal pathogens, is implicated in the initiation and progression of periodontal disease. The initial stages of periodontal inflammation are accompanied by vascular hyperpermeability. In our present study, we report that the P. gingivalis lipopolysaccharide (LPS) increases the mRNA expression of interleukin-8 (IL-8), a major inducer of vascular permeability, in vascular endothelial cells. P. gingivalis LPS also stimulated the induction of IL-8 secretion in endothelial cells. The P. gingivalis LPS-induced expression of IL-8 was primarily modulated by nuclear factor-kappaB (NF-kappaB). P. gingivalis LPS significantly enhanced the vascular permeability both in vitro and in vivo, and a blockade of the IL-8 receptor decreased the P. gingivalis LPS-induced vascular permeability. Taken together, these results suggest that P. gingivalis LPS increases vascular permeability through the NF-kappaB-dependent production of IL-8 in vascular endothelial cells.
