Description:
<jats:title>ABSTRACT</jats:title>
<jats:p>
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,
<jats:italic>Streptococcus cristatus</jats:italic>
and
<jats:italic>Porphyromonas gingivalis</jats:italic>
. A surface protein of
<jats:italic>S. cristatus</jats:italic>
caused repression of the
<jats:italic>P. gingivalis</jats:italic>
fimbrial gene (
<jats:italic>fimA</jats:italic>
), as determined by a chromosomal
<jats:italic>fimA</jats:italic>
promoter-
<jats:italic>lacZ</jats:italic>
reporter construct and by reverse transcription-PCR. Signaling activity was associated with a 59-kDa surface protein of
<jats:italic>S. cristatus</jats:italic>
and showed specificity for the
<jats:italic>fimA</jats:italic>
gene. Furthermore,
<jats:italic>P. gingivalis</jats:italic>
was unable to form biofilm microcolonies with
<jats:italic>S. cristatus</jats:italic>
. Thus,
<jats:italic>S. cristatus</jats:italic>
is capable of modulating virulence gene expression in
<jats:italic>P. gingivalis</jats:italic>
, consequently influencing the development of pathogenic plaque.
</jats:p>