期刊
JOURNAL OF BACTERIOLOGY
卷 182, 期 24, 页码 7067-7069出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JB.182.24.7067-7069.2000
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资金
- NIDCR NIH HHS [K08 DE00401, DE10595, R01 DE012505, DE12505, P60 DE013061] Funding Source: Medline
Dental plaque is a complex biofilm that accretes in a series of discrete steps proceeding from a gram-positive streptococcus-rich biofilm to a structure rich in gram-negative anaerobes. This study investigated information flow between two unrelated plaque bacteria, Streptococcus cristatus and Porphyromonas gingivalis. A surface protein of S. cristatus caused repression of the P. gingivalis fimbrial gene (fimA), as determined by a chromosomal fimA promoter-lacZ reporter construct and by reverse transcription-PCR Signaling activity was associated with a 59-kDa surface protein of S. cristatus and showed specificity for the fimA gene. Furthermore, P. gingivalis was unable to form biofilm microcolonies with S. cristatus. Thus, S. cristatus is capable of modulating virulence gene expression in P. gingivalis, consequently influencing the development of pathogenic plaque.
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