Possible Roles of IL-33 in Periodontal Diseases: Porphyromonas gingivalis Induced IL-33 in Human Gingival Epithelial Cells

ABSTRACT Porphyromonas gingivalis, one of the causative agents of adult periodontitis, can invade and survive within host epithelial cells. The molecular mechanisms by which P. gingivalis induces uptake and adapts to an intracellular environment are not fully understood. In this study, we have investigated the genetic responses of P. gingivalis internalized within human gingival epithelial cells (GECs) in order to identify factors involved in invasion and survival. We compared the differential display of arbitrarily PCR-amplified gene transcripts in P. gingivalis recovered from GECs with the display of transcripts in P. gingivalis control cultures. Over 20 potential differentially expressed transcripts were identified. Among these, pepO, encoding an endopeptidase, and genes encoding an ATP-binding cassette (ABC) transporter and a cation-transporting ATPase were upregulated in GECs. To investigate the functionality of these gene products, mutants were generated by insertional inactivation. Compared to the parental strain, mutants of each gene showed a significant reduction in their invasion capabilities. In addition, GEC cytoskeletal responses to the mutants were distinct from those induced by the parent. In contrast, adhesion of the mutant strains to GECs was not affected by lack of expression of the gene products. These results suggest that PepO, a cation-transporting ATPase, and an ABC transporter are required for the intracellular lifestyle of P. gingivalis.

Download Full-text

PR055: Porphyromonas gingivalis modulates cell proliferation of human gingival epithelial cells by skp2/p21

Journal Of Clinical Periodontology ◽

10.1111/jcpe.54_12915 ◽

2018 ◽

Vol 45 ◽

pp. 137-138

Keyword(s):

Cell Proliferation ◽

Epithelial Cells ◽

Porphyromonas Gingivalis ◽

Gingival Epithelial Cells ◽

Human Gingival Epithelial Cells

Download Full-text

Porphyromonas gingivalis traffics into endoplasmic reticulum-rich-autophagosomes for successful survival in human gingival epithelial cells

Virulence ◽

10.1080/21505594.2018.1454171 ◽

2018 ◽

Vol 9 (1) ◽

pp. 845-859 ◽

Cited By ~ 28

Author(s):

Kyulim Lee ◽

JoAnn S. Roberts ◽

Chul Hee Choi ◽

Kalina R. Atanasova ◽

Özlem Yilmaz

Keyword(s):

Endoplasmic Reticulum ◽

Epithelial Cells ◽

Porphyromonas Gingivalis ◽

Gingival Epithelial Cells ◽

Human Gingival Epithelial Cells

Download Full-text

Detectable Dioxins in Human Saliva and Their Effects on Gingival Epithelial Cells

Journal of Dental Research ◽

10.1177/154405910308201017 ◽

2003 ◽

Vol 82 (10) ◽

pp. 849-853 ◽

Cited By ~ 6

Author(s):

T. Ogawa ◽

Y. Asai ◽

M. Yamashita ◽

T. Takasuga

Keyword(s):

Epithelial Cells ◽

Periodontal Diseases ◽

Human Saliva ◽

World Health ◽

Pathogenic Factor ◽

Gingival Epithelial Cells ◽

Coplanar Polychlorinated Biphenyls ◽

Blood Specimens ◽

Human Gingival Epithelial Cells ◽

Health Organization

Dioxin, a powerful hormone-disrupting chemical, exhibits serious health effects when it reaches body fat. Here we analyzed coplanar polychlorinated biphenyls (PCBs) and polychlorinated-dibenzo- p-dioxins (PCDDs) in human saliva as compared with blood specimens, and examined their effects on human gingival epithelial cells (HGEC). High levels of tri- and tetrachlorinated PCBs were found in saliva, whereas we detected predominantly hexa- and heptachlorinated PCBs in blood. Among PCDDs, the saliva and blood specimens contained mainly 1,2,3,4,6,7,8,9-octachlorodibenzo- p-dioxin (OCDD). Among the toxic dioxins proposed by the World Health Organization (WHO) in 1998, 2,3′,4,4′,5-pentachlorobiphenyl (PCB 118) and OCDD, which were mainly found in saliva, significantly induced IL-8 production in HGEC. Furthermore, these two dioxins markedly augmented IL-8 production stimulated with fimbriae from Porphyromonas gingivalis, which is well-known as a pathogenic factor in periodontal diseases. These results suggest that dioxins in saliva may be a risk factor for periodontal diseases.

Download Full-text