N-acetylcysteine and the human serum components that inhibit bacterial invasion of gingival epithelial cells prevent experimental periodontitis in mice.
10.5051/jpis.2014.44.6.266
- Author:
Jehan ALAM
1
;
Keum Jin BAEK
;
Yun Sik CHOI
;
Yong Cheol KIM
;
Youngnim CHOI
Author Information
1. Department of Oral Microbiology and Immunology, Dental Research Institute, Seoul National University School of Dentistry, Seoul, Korea. youngnim@snu.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Albumins;
Bacteria;
Epithelial cells;
Immunoglobulin G;
Periodontitis
- MeSH:
Acetylcysteine*;
Actin Cytoskeleton;
Albumins;
Alveolar Bone Loss;
Animals;
Bacteria;
Bacterial Adhesion;
Epithelial Cells*;
Flow Cytometry;
Fusobacterium nucleatum;
Humans;
Immunoglobulin G;
Mice*;
Monomeric GTP-Binding Proteins;
Periodontitis*;
Porphyromonas gingivalis;
Reactive Oxygen Species;
Serum Albumin
- From:Journal of Periodontal & Implant Science
2014;44(6):266-273
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: We previously reported that human serum significantly reduces the invasion of various oral bacterial species into gingival epithelial cells in vitro. The aims of the present study were to characterize the serum component(s) responsible for the inhibition of bacterial invasion of epithelial cells and to examine their effect on periodontitis induced in mice. METHODS: Immortalized human gingival epithelial (HOK-16B) cells were infected with various 5- (and 6-) carboxy-fluorescein diacetate succinimidyl ester-labeled oral bacteria, including Fusobacterium nucleatum, Provetella intermedia, Porphyromonas gingivalis, and Treponiema denticola, in the absence or presence of three major serum components (human serum albumin [HSA], pooled human IgG [phIgG] and alpha1-antitrypsin). Bacterial adhesion and invasion were determined by flow cytometry. The levels of intracellular reactive oxygen species (ROS) and activation of small GTPases were examined. Experimental periodontitis was induced by oral inoculation of P. gingivalis and T. denticola in Balb/c mice. RESULTS: HSA and phIgG, but not alpha1-antitrypsin, efficiently inhibited the invasion of various oral bacterial species into HOK-16B cells. HSA but not phIgG decreased the adhesion of F. nucleatum onto host cells and the levels of intracellular ROS in HOK-16B cells. N-acetylcysteine (NAC), a ROS scavenger, decreased both the levels of intracellular ROS and invasion of F. nucleatum into HOK-16B cells, confirming the role of ROS in bacterial invasion. Infection with F. nucleatum activated Rac1, a regulator of actin cytoskeleton dynamics. Not only HSA and NAC but also phIgG decreased the F. nucleatum-induced activation of Rac1. Furthermore, both HSA plus phIgG and NAC significantly reduced the alveolar bone loss in the experimental periodontitis induced by P. gingivalis and T. denticola in mice. CONCLUSIONS: NAC and the serum components HSA and phIgG, which inhibit bacterial invasion of oral epithelial cells in vitro, can successfully prevent experimental periodontitis.
