Streptococcus cristatus attenuates Fusobacterium nucleatum-induced interleukin-8 expression in oral epithelial cells.
Streptococcus cristatus attenuates Fusobacterium nucleatum-induced interleukin-8 expression in oral epithelial cells.
复制标题
冠状链球菌减弱具核梭杆菌诱导的口腔上皮细胞中白细胞介素 8 的表达。
DOI:
10.1111/j.1600-0765.2007.01057.x
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发表时间:
2008
影响因子:
3.5
通讯作者:
Rudney,JD
中科院分区:
文献类型:
--
作者:
Zhang,G;Chen,R;Rudney,JD
Background and Objective:Oral epithelial cells may be invaded by a polymicrobial intracellular flora, including pathogens together with commensals. Various oral pathogens can induce the production of interleukin‐8, a potent neutrophil chemotractant, in oral epithelial cells. Evidence from the gut suggests that commensal species may modulate inflammatory responses to pathogens. The aim of this study was to examine the interleukin‐8 responses of oral epithelial cells to an oral pro‐inflammatory species,Fusobacterium nucleatum, in combination with an oral commensal,Streptococcus cristatus.Material and methods:KB, TERT‐2, TR146 and SCC15 cells were cocultured withF. nucleatumandS. cristatus, either alone or in combination, at 37°C in 5% CO2under various conditions. The mRNA expression of interleukin‐8 was analyzed by reverse transcription–polymerase chain reaction and protein secretion was measured by enzyme‐linked immunosorbent assay.Results:F. nucleatumalone evoked a potent interleukin‐8 response, whereasS. cristatusalone did not induce significant interleukin‐8 expression in oral epithelial cells. When present together,S. cristatusattenuated theF. nucleatum‐induced interleukin‐8 production in the four oral epithelial cell lines to varying degrees. The inhibitory effect ofS. cristatuswas independent of its viability and its co‐aggregation withF. nucleatum, was not related to soluble bacterial products and appeared to require bacterial contact with epithelial cells. Similar effects were seen with several other species of oral streptococci.Conclusion:Our data suggest thatS. cristatusmay exert immunomodulatory effects on the interleukin‐8 response of oral epithelial cells toF. nucleatumchallenge.