Molecular mechanisms of compounds affecting bacterial biofilm formation and dispersal.
ABSTRACT Bacteria can switch between planktonic forms (single cells) and biofilms, i.e., bacterial communities growing on solid surfaces and embedded in a matrix of extracellular polymeric substance. Biofilm formation by pathogenic bacteria often results in lower susceptibility to antibiotic treatments and in the development of chronic infections; thus, biofilm formation can be considered an important virulence factor. In recent years, much attention has been directed towards understanding the biology of biofilms and towards searching for inhibitors of biofilm development and of biofilm-related cellular processes. In this report, we review selected examples of target-based screening for anti-biofilm agents: We focus on inhibitors of quorum sensing, possibly the most characterized target for molecules with anti-biofilm activity, and on compounds interfering with the metabolism of the signal molecule cyclic di-GMP metabolism and on inhibitors of DNA and nucleotide biosynthesis, which represent a novel and promising class of biofilm inhibitors. Finally, we discuss the activation of biofilm dispersal as a novel mode of action for anti-biofilm compounds.
- SourceAvailable from: Murugan Kasi
Dataset: SJBS urinary tract biofilm
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ABSTRACT: The transition between planktonic growth and biofilm formation represents a tightly regulated developmental shift that has substantial impact on cell fate. Here, we highlight different mechanisms through which bacteria limit their own biofilm development. The mechanisms involved in these self-inhibition processes include: (i) regulation by secreted small molecules, which govern intricate signaling cascades that eventually decrease biofilm development, (ii) extracellular polysaccharides capable of modifying the physicochemical properties of the substratum, and (iii) extracellular DNA that masks an adhesive structure. These mechanisms, which rely on substances produced by the bacterium and released into the extracellular milieu, suggest regulation at the communal level. In addition, we provide specific examples of environmental cues (e.g. blue-light or glucose level) that trigger a cellular response reducing biofilm development. All together, we describe a diverse array of mechanisms underlying self-inhibition of biofilm development in different bacteria, and discuss possible advantages of these processes.Environmental Microbiology 08/2014; 17(5). DOI:10.1111/1462-2920.12583 · 6.24 Impact Factor
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ABSTRACT: Two cobalt imidazolate metal–organic frameworks were evaluated as a bactericidal material against the growt h of the Gram-negative bacteria Pseudomonas putida and Escherichia coli. Under the most unfavourable conditions, within the exponential growth phase and in the culture media for both microorganisms, the growth inhibition reached over 50% for concentrations of biocidal material in the 5–10 mg L�-1 range. The release of metal gives excellent durability with the antibacterial effect persisting after 3 months. Both cobalt-based materials can be prepared with simple, cheap and easily accessible commercial ligands, leading to a more affordable possible future application as antimicrobial materials.Chemosphere 06/2014; 113:188-192. DOI:10.1016/j.chemosphere.2014.05.029 · 3.50 Impact Factor