Inhibition of biofilm formation of periodontal pathogens by D-arabinose
1
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
Periodontitis and periimplantitis are caused as a result of dental biofilm formation. This biofilm is composed of multiple species of pathogens. Therefore, controlling biofilm formation is critical for disease prevention. To inhibit biofilm formation, sugars can be used to interrupt lectin-involving interactions between bacteria or between bacteria and a host. In this study, we evaluated the effect of D-Arabinose on biofilm formation of putative periodontal pathogens as well as the quorum sensing activity and whole protein profiles of the pathogens. Crystal violet staining, confocal laser scanning microscopy, and scanning electron microscopy revealed that D-Arabinose inhibited biofilm formation of Porphyromonas gingivalis , Fusobacterium nucleatum , and Tannerella forsythia . D-Arabinose also significantly inhibited the activity of autoinducer 2 of F. nucleatum and the expression of representative bacterial virulence genes. Furthermore, D-Arabinose treatment altered the expression of some bacterial proteins. These results demonstrate that D-Arabinose can be used as an antibiofilm agent for the prevention of periodontal infections.
Abstract
Periodontitis and periimplantitis are caused as a result of dental biofilm formation. This biofilm is composed of multiple species of pathogens. Therefore, controlling biofilm formation is critical for disease prevention. To inhibit biofilm formation, sugars can be used to interrupt lectin-involving interactions between bacteria or between bacteria and a host. In this study, we evaluated the effect of D-Arabinose on biofilm formation of putative periodontal pathogens as well as the quorum sensing activity and whole protein profiles of the pathogens. Crystal violet staining, confocal laser scanning microscopy, and scanning electron microscopy revealed that D-Arabinose inhibited biofilm formation of Porphyromonas gingivalis , Fusobacterium nucleatum , and Tannerella forsythia . D-Arabinose also significantly inhibited the activity of autoinducer 2 of F. nucleatum and the expression of representative bacterial virulence genes. Furthermore, D-Arabinose treatment altered the expression of some bacterial proteins. These results demonstrate that D-Arabinose can be used as an antibiofilm agent for the prevention of periodontal infections.
참고문헌 (22)
- Daubert DM, "Biofilm as a risk factor in implant treatment", Periodontol 2000, 81, pp.29~40 (2019)[DOI]
- de Melo F, "A systematic review of the microbiota composition in various periimplant conditions : data from 16S rRNA gene sequencing", Arch Oral Biol, 117, pp.104776~ (2020)[DOI]
- Griffen AL, "Distinct and complex bacterial profiles in human periodontitis and health revealed by 16S pyrosequencing", ISME J, 6, pp.1176~1185 (2012)[DOI]
- Haffajee AD, "Microbial etiological agents of destructive periodontal diseases", Periodontol 2000, 5, pp.78~111 (1994)[DOI]
- Hajishengallis G, "Local and systemic mechanisms linking periodontal disease and inflammatory comorbidities", Nat Rev Immunol, 21, pp.426~440 (2021)[DOI]
- Xu S, "Associations between osteoporosis and risk of periodontitis : a pooled analysis of observational studies", Oral Dis, 27, pp.357~369 (2021)[DOI]
- Roy R, "Strategies for combating bacterial biofilms : a focus on anti-biofilm agents and their mechanisms of action", Virulence, 9, pp.522~554 (2018)[DOI]
- Sintim HO, "and bacterial eradication", OMICS, 20, pp.3~11 (2016)[DOI]
- Rickard AH, "Bacterial coaggregation : an integral process in the development of multi-species biofilms", Trends Microbiol, 11, pp.94~100 (2003)[DOI]
- Stevens MR, "Coaggregation occurs between microorganisms isolated from different environments", FEMS Microbiol Ecol, 91, pp.fiv123~ (2015)[DOI]
- Kolenbrander PE, "Inhibition of coaggregation between Fusobacterium nucleatum and Porphyromonas(Bacteroides)gingivalis by lactose and related sugars", Infect Immun, 57, pp.3204~3209 (1989)[DOI]
- Kolenbrander PE, "Coaggregation of Fusobacterium nucleatum, Selenomonas flueggei, Selenomonas infelix, Selenomonas noxia, and Selenomonas sputigena with strains from 11 genera of oral bacteria", Infect Immun, 57, pp.3194~3203 (1989)[DOI]
- Rutherford ST, "Bacterial quorum sensing : its role in virulence and possibilities for its control", Cold Spring Harb Perspect Med, 2, pp.a012427~ (2012)[DOI]
- Taga ME, "Chemical communication among bacteria", Proc Natl Acad Sci U S A, 100(Suppl 2), pp.14549~14554 (2003)[DOI]
- James D, "The Actinobacillus actinomycetemcomitans ribose binding protein RbsB interacts with cognate and heterologous autoinducer 2 signals", Infect Immun, 74, pp.4021~4029 (2006)[DOI]
- Jang YJ, "Autoinducer 2 of Fusobacterium nucleatum as a target molecule to inhibit biofilm formation of periodontopathogens", Arch Oral Biol, 58, pp.17~27 (2013)[DOI]
- Eun-Ju Ryu, "D-Galactose as an autoinducer 2 inhibitor to control the biofilm formation of periodontopathogens", The Journal of Microbiology, 54(9), pp.632~637 (2016), 한국미생물학회[DOI]
- Rubinstein MR, "Fusobacterium nucleatum promotes colorectal carcinogenesis by modulating E-cadherin", β-catenin signaling via its FadA adhesin, 2013, pp.14, 195~206
- Sakanaka A, "Dual lifestyle of Porphyromonas gingivalis in biofilm and gingival cells", Microb Pathog, 94, pp.42~47 (2016)[DOI]
- Sharma A, "Virulence mechanisms of Tannerella forsythia", Periodontol 2000, 54, pp.106~116 (2010)[DOI]
- Sharma A, "Synergy between Tannerella forsythia and Fusobacterium nucleatum in biofilm formation", Oral Microbiol Immunol, 20, pp.39~42 (2005)[DOI]
- Young-Jong Lee, "Inhibitory Effect of Pentose on Biofilm Formation by Oral Bacteria", International Journal of Oral Biology, 35(4), pp.203~207 (2010), 대한구강생물학회