The oral commensal Streptococcus mitis activates the aryl hydrocarbon receptor in human oral epithelial cells  

作　　者：stian a engen gro h rørvik olav schreurs inger js blix karl schenck Stian A Engen Gro H Rorvik Olav Schreurs Inger JS Blix Karl Schenck(Department of Oral Biology, Faculty of Dentistry, University of Oslo, Oslo, Norway Institute of Clinical Dentistry, Faculty of Dentistry, University of Oslo, Osfo, Norway Correspondence,Dr SA Engen, Department of Oral Biology, Faculty of Dentistry, University of Oslo, PB 1052 Blindern, Oslo N-0316, Norway)

机构地区：[1]department of oral biology,faculty of dentistry,university of oslo,Oslo,Norway [2]institute of clinical dentistry,faculty of dentistry,university of oslo,Oslo,Norway

出　　处：《International Journal of Oral Science》2017年第3期145-150,共6页国际口腔科学杂志（英文版）

基　　金：supported by the Norwegian Research Council grant no.241011;the Norwegian Dental Depot Fund for Dental Research

摘　　要：Streptococcus mitis （S. mitis） is a pioneer commensal bacterial species colonizing many of the surfaces of the oral cavity in healthy individuals. Yet, not much information is available regarding its interaction with the host. We used examination of its transcriptional regulation in oral keratinocytes to elucidate some of its potential roles in the oral cavity. Transcription factor analysis of oral keratinocytes predicted S. mitis.mediated activation of aryl hydrocarbon receptor （AhR）, Activation and functionality of AhR was confirmed through nuclear translocation determined by immunofluorescence microscopy and real-time polymerase chain reaction with reverse transcription analysis of CYPIA1, the hallmark gene for AhR activation. Addition of Streptococcus mutans or Streptococcus gordonfi did not induce CYPIA1 transcription in the keratinocyte cultures. Introduction of an AhR-specific inhibitor revealed that S. mitis-mediated transcription of CXCL2 and CXCL8 was regulated by AhR. Elevated levels of pmstaglandin E2 （enzyme-linked immunosorbent assay） in supernatants from S. mitis-treated oral epithelial cells were also attenuated by inhibition of AhR activity. The observed AhR-regulated activities point to a contribution of S. mitis in the regulation of inflammatory responses and thereby to wound healing in the oral cavity. The concept that the oral commensal microbiota can induce AhR activation is important, also in view of the role that AhR has in modulation of T-cell differentiation and as an anti-inflammatory factor in macrophaees.Streptococcus mitis （S. mitis） is a pioneer commensal bacterial species colonizing many of the surfaces of the oral cavity in healthy individuals. Yet, not much information is available regarding its interaction with the host. We used examination of its transcriptional regulation in oral keratinocytes to elucidate some of its potential roles in the oral cavity. Transcription factor analysis of oral keratinocytes predicted S. mitis.mediated activation of aryl hydrocarbon receptor （AhR）, Activation and functionality of AhR was confirmed through nuclear translocation determined by immunofluorescence microscopy and real-time polymerase chain reaction with reverse transcription analysis of CYPIA1, the hallmark gene for AhR activation. Addition of Streptococcus mutans or Streptococcus gordonfi did not induce CYPIA1 transcription in the keratinocyte cultures. Introduction of an AhR-specific inhibitor revealed that S. mitis-mediated transcription of CXCL2 and CXCL8 was regulated by AhR. Elevated levels of pmstaglandin E2 （enzyme-linked immunosorbent assay） in supernatants from S. mitis-treated oral epithelial cells were also attenuated by inhibition of AhR activity. The observed AhR-regulated activities point to a contribution of S. mitis in the regulation of inflammatory responses and thereby to wound healing in the oral cavity. The concept that the oral commensal microbiota can induce AhR activation is important, also in view of the role that AhR has in modulation of T-cell differentiation and as an anti-inflammatory factor in macrophaees.

关 键 词：aryl hydrocarbon receptor COMMENSAL INFLAMMATION oral epithelium prostaglandin E2 STREPTOCOCCUS 

分 类 号：R780.2[医药卫生—口腔医学]