Control of Polymicrobial Biofilms: Recent Trends - Antibiofilm Agents: From Diagnosis to Treatment and Prevention - page 330

not only unable to form substantial biofilms with M. luteus 2.13, but it was also
impaired in forming single-species biofilms suggesting a dual role for
coaggregation (cell-surface adhesion and cell-cell adhesion/coaggregation).
Thus, coaggregation could be targeted to prevent initial and later colonizing events
in biofilms. Considering the difficulties in treating freshwater biofilms and the
potential for pathogens or problematic organisms that reside in freshwater biofilms
in public, industrial, and healthcare settings (Exner et al. 2005 ; Simoes et al. 2008 ;
Declerck 2010 ; Vornhagen et al. 2013 ), such an approach to inhibit pathogen
integration that do not require the use of antimicrobials is extremely attractive.
Coaggregation may have potential to be used in a more manipulative fashion,
within polymicrobial biofilm communities. It is possible that the use of a
coaggregating organism that is antagonistic to pathogens will represent a guerrilla
warfare approach to preventing the colonization or expansion of pathogenic
populations in polymicrobial biofilms. For example, building upon early work by
Reid and coworkers ( 1988 ), recent work by Younes et al. ( 2012 ) has raised the
potential utility of coaggregation as a tool to manipulate urogenital biofilm com-
munities. Specifically, coaggregating urogenital lactobacilli have been shown to
coaggregate with urogenital pathogens and inactivate their pathogenic potential
(Reid et al. 1988 ; Reid and Burton 2002 ; Younes et al. 2012 ). Younes and
colleagues stated that coaggregation “creates a hostile microenvironment around
a pathogen. With antimicrobial options fading, it therewith becomes increasingly
important to identify lactobacilli that bind strongly with pathogens” (Younes
et al. 2012 ).
Unfortunately, approaches to use coaggregation to control polymicrobial
biofilms have yet to gain substantial traction. This is likely because coaggregation
was originally considered to be a phenomenon unique to the human oral cavity
(Handely et al. 2001 ). Not until the mid-1990s did coaggregation begin to receive
attention by researchers in other fields, and this attention has since accelerated
(Vandevoorde et al. 1992 ; Kmet et al. 1995 ; Drago et al. 1997 ; Kmet and Lucchini
1997 ; Egwari et al. 2000 ; Rickard et al. 2002 ; Malik and Kakii 2003 ; Edwards
et al. 2006 ; Hill et al. 2010 ). This is in part likely driven by increasing interest in
polymicrobial biofilm communities and the developmental processes that lead to
their development. It has now become increasingly clear that the vast majority of
coaggregation interactions between bacteria are mediated by protein lectin-like
adhesins and receptor polysaccharides on partner cells (Rickard et al. 2003 ). In
many instances, coaggregation can be inhibited by the addition of simple sugars or
chelating agents such as EDTA—which presumably results in competitive inhibi-
tion and the alteration of structure, respectively, of receptor polysaccharides. While
yet to be evaluated in complex polymicrobial communities, it is possible that the
addition of sugars or chelators, that inhibit coaggregation, may retard biofilm
development. Further stressing the importance of coaggregation and the possible
usefulness of inhibiting the activity of adhesins or receptors, de Toleedo and
colleagues ( 2012 ) reported that oral S. oralis coaggregation receptor polysaccha-
rides induce inflammatory responses in human aortic endothelial cells and may
contribute to the development of infective endocarditis and atherosclerosis, both of