Dietary plant components ellagic acid and tannic acid inhibit Escherichiacoli biofilm formation
Author(s) -
Viktoria Hancock,
Malin Dahl,
Rebecca Munk Vejborg,
Per Klemm
Publication year - 2009
Publication title -
journal of medical microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.91
H-Index - 117
eISSN - 1473-5644
pISSN - 0022-2615
DOI - 10.1099/jmm.0.013680-0
Subject(s) - tannic acid , ellagic acid , biofilm , microbiology and biotechnology , extant taxon , biology , chemistry , biochemistry , bacteria , botany , polyphenol , genetics , evolutionary biology , antioxidant
Bacteria usually live as surface-associated communities, rather than as planktonic cells. These compact microbial consortia, referred to as biofilms, are commonly associated with many health problems (Costerton et al., 1999; Donlan, 2002). A few common examples of where biofilms form are in dental plaque, in lung infections and in infections related to the use of medical devices, such as catheters. Many persistent and chronic bacterial infections are now thought to be linked to biofilm formation; more than 60 % of all bacterial infections have been estimated to involve biofilm formation (Lewis, 2001). Virtually all medical implants are prone to colonization and biofilm formation by pathogenic bacteria, and such biofilms can serve as a source for recurrent infections (Costerton et al., 1999). Biofilm-linked infections are particularly problematic, because biofilm-associated bacteria can tolerate immune defences, antibiotics, biocides and hydrodynamic shear forces far better than the corresponding planktonic bacteria. The intrinsic tolerance of biofilm-associated bacteria towards antimicrobial agents makes biofilmassociated infections particularly recalcitrant toward treatment. New types of antibiotics are therefore needed; development of candidate drugs that target biofilm formation will be of great importance. Most conventional antibiotics have targeted biochemical and physiological functions that are present both in pathogenic as well as saprophytic bacteria. Specific targeting of diseaseassociated bacterial lifestyles such as biofilm formation but not free-living pelagic bacteria is a highly attractive approach that has not yet been exploited. Drugs specifically aimed at bacterial biofilm formation are unlikely to be crossresistant to existing therapies.
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