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Conference Paper: Commensals and periodontopathogens modulate immuno-inflammatory trajectories in HOKs and THP-1

TitleCommensals and periodontopathogens modulate immuno-inflammatory trajectories in HOKs and THP-1
Authors
KeywordsBacterial
Host-microbial interactions
Inflammatory mediators
Periodontal disease and Periodontal organisms
Issue Date2012
PublisherSage Publications, Inc.. The Journal's web site is located at http://www.sagepub.com/journalsProdDesc.nav?prodId=Journal201925
Citation
The Annual Meeting of the International Association for Dental Research (IADR) Southeast Asian Division, Hong Kong, China, 3-4 November 2012. In Journal of Dental Research, 2012, v. 91 n. Special Issue C: abstract no. 169577 How to Cite?
AbstractObjectives: Periodontal disease is initiated from pathogenic bacteria-mediated uncoordinated inflammatory host response. However, whether commensals and pathogens follow different trajectories during their interactions with host cells is largely unknown. The present study aimed to examine the crosstalk of commensals and periodontopathogens in human oral keratinocytes (HOKs) and THP-1 monocytes. Methods: The commensal oral bacteria including Streptococcus mutans (Sm), Streptococcus mitis (Smi) and Streptococcus sanguinis (Ss), and periodontopathogens including Aggregatibacter actinomycetemcomitans (Aa) and Porphyromonas gingivalis (Pg) were Selected. The interaction of bacteria with HOKs and THP-1 cells was analyzed in a co-culture model using a gradient of multiplicity of infection. The expression of IL-1b, IL-6, IL-8 and TNF-¦Á was assessed using ELISA and real-time qPCR. Cell surface receptors and signal transduction pathways were examined by western blots, and antibody-mediated blocking assays were undertaken for analysis of TLR2 and TLR4. Results: The commensals upregulated the pro-inflammatory cytokines expression in both HOKs and THP-1 monocytes. In contrast, periodontopathogens induced higher levels of cytokines expression in HOKs, while in monocytes Pg down-regulated the TLR-mediated immuno-inflammatory response. THP-1 was more responsive to Smi and Ss in terms of IL-8 and TNF-¦Á production, and to Sm and Smi in terms of IL-1b than the controls and that treated with Pg (p<0.05). In HOKs, both Sm and Pg upregulated IL-6 and IL-8 expression as compared with the control (p<0.05). The cytokines expressions was through TLRs-mediated downstream pathways. Conclusions : It seems that HOKs enable to detect the trajectories of oral commensal and pathogenic bacteria. However, once the periodontopathogens like Pg breach the epithelial barrier they may evade the host defense by paralysing the pro-inflammatory cytokine network of immune cells such as monocytes, thereby achieving proliferation in gingival tissues and contributing to periodontal disease.
DescriptionSession: Periodontal Research
Persistent Identifierhttp://hdl.handle.net/10722/182065
ISSN
2015 Impact Factor: 4.602
2015 SCImago Journal Rankings: 1.714

 

DC FieldValueLanguage
dc.contributor.authorLi, Hen_US
dc.contributor.authorSeneviratne, CJen_US
dc.contributor.authorLau, ASen_US
dc.contributor.authorWang, CYen_US
dc.contributor.authorJin, Len_US
dc.date.accessioned2013-04-17T07:20:44Z-
dc.date.available2013-04-17T07:20:44Z-
dc.date.issued2012en_US
dc.identifier.citationThe Annual Meeting of the International Association for Dental Research (IADR) Southeast Asian Division, Hong Kong, China, 3-4 November 2012. In Journal of Dental Research, 2012, v. 91 n. Special Issue C: abstract no. 169577en_US
dc.identifier.issn0022-0345-
dc.identifier.urihttp://hdl.handle.net/10722/182065-
dc.descriptionSession: Periodontal Research-
dc.description.abstractObjectives: Periodontal disease is initiated from pathogenic bacteria-mediated uncoordinated inflammatory host response. However, whether commensals and pathogens follow different trajectories during their interactions with host cells is largely unknown. The present study aimed to examine the crosstalk of commensals and periodontopathogens in human oral keratinocytes (HOKs) and THP-1 monocytes. Methods: The commensal oral bacteria including Streptococcus mutans (Sm), Streptococcus mitis (Smi) and Streptococcus sanguinis (Ss), and periodontopathogens including Aggregatibacter actinomycetemcomitans (Aa) and Porphyromonas gingivalis (Pg) were Selected. The interaction of bacteria with HOKs and THP-1 cells was analyzed in a co-culture model using a gradient of multiplicity of infection. The expression of IL-1b, IL-6, IL-8 and TNF-¦Á was assessed using ELISA and real-time qPCR. Cell surface receptors and signal transduction pathways were examined by western blots, and antibody-mediated blocking assays were undertaken for analysis of TLR2 and TLR4. Results: The commensals upregulated the pro-inflammatory cytokines expression in both HOKs and THP-1 monocytes. In contrast, periodontopathogens induced higher levels of cytokines expression in HOKs, while in monocytes Pg down-regulated the TLR-mediated immuno-inflammatory response. THP-1 was more responsive to Smi and Ss in terms of IL-8 and TNF-¦Á production, and to Sm and Smi in terms of IL-1b than the controls and that treated with Pg (p<0.05). In HOKs, both Sm and Pg upregulated IL-6 and IL-8 expression as compared with the control (p<0.05). The cytokines expressions was through TLRs-mediated downstream pathways. Conclusions : It seems that HOKs enable to detect the trajectories of oral commensal and pathogenic bacteria. However, once the periodontopathogens like Pg breach the epithelial barrier they may evade the host defense by paralysing the pro-inflammatory cytokine network of immune cells such as monocytes, thereby achieving proliferation in gingival tissues and contributing to periodontal disease.-
dc.languageengen_US
dc.publisherSage Publications, Inc.. The Journal's web site is located at http://www.sagepub.com/journalsProdDesc.nav?prodId=Journal201925-
dc.relation.ispartofJournal of Dental Researchen_US
dc.rightsJournal of Dental Research. Copyright © Sage Publications, Inc..-
dc.subjectBacterial-
dc.subjectHost-microbial interactions-
dc.subjectInflammatory mediators-
dc.subjectPeriodontal disease and Periodontal organisms-
dc.titleCommensals and periodontopathogens modulate immuno-inflammatory trajectories in HOKs and THP-1en_US
dc.typeConference_Paperen_US
dc.identifier.emailSeneviratne, CJ: jaya@hku.hken_US
dc.identifier.emailJin, L: ljjin@hkucc.hku.hken_US
dc.identifier.authoritySeneviratne, CJ=rp01372en_US
dc.identifier.authorityJin, L=rp00028en_US
dc.identifier.hkuros213913en_US
dc.identifier.volume91en_US
dc.identifier.issueSpecial Issue C: abstract no. 169577en_US
dc.publisher.placeUnited States-

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