Biofilm

About: Biofilm is a research topic. Over the lifetime, 23010 publications have been published within this topic receiving 906812 citations. The topic is also known as: biofilms.

The RcsC sensor kinase is required for normal biofilm formation in Escherichia coli K-12 and controls the expression of a regulon in response to growth on a solid surface.

Abstract: Summary Bacteria are often found associated with surfaces as sessile bacterial communities called biofilms, and the formation of a biofilm can be split up into different stages each requiring the expression of specific genes. The production of extracellular polysaccharides (EPS) is important for the maturation of biofilms and is controlled by the Rcs two-component pathway in Escherichia coli (and other Gram-negative bacteria). In this study, we show, for the first time, that the RcsC sensor kinase is required for normal biofilm development in E. coli. Moreover, using a combination of DNA macroarray technology and transcriptional fusion analysis, we show that the expression of > 150 genes is controlled by RcsC in E. coli. In silico analyses of the RcsC regulon predicts that 50% of the genes encode proteins that are either localized to the envelope of E. coli or have activities that affect the structure/properties of the bacterial surface, e.g. the production of colanic acid. Moreover, we also show that RcsC is activated during growth on a solid surface. Therefore, we suggest that the RcsC sensor kinase may play an important role in the remodelling of the bacterial surface during growth on a solid surface and biofilm formation.

YliH (BssR) and YceP (BssS) Regulate Escherichia coli K-12 Biofilm Formation by Influencing Cell Signaling

Abstract: We previously discovered that yliH and yceP are induced in Escherichia coli biofilms (D. Ren, L. A. Bedzyk, S. M. Thomas, R. W. Ye, and T. K. Wood, Appl. Microbiol. Biotechnol. 64:515-524, 2004). Here, it is shown that deletion of yceP (b1060) and yliH (b0836) increases biofilm formation in continuous-flow chambers with minimal glucose medium by increasing biofilm mass (240- to 290-fold), surface coverage (16- to 31-fold), and mean thickness (2,800-fold). To determine the genetic basis of the increase in biofilm formation, we examined the differential gene expression profile in biofilms for both the mutants relative to the wild-type strain in rich medium with glucose and found that 372 to 882 genes were induced and that 76 to 337 were repressed consistently >2-fold (P ≤ 0.05). The increase in biofilm formation was related to differential expression of genes related to stress response (8 to 64 genes) for both mutants, including rpoS and sdiA. More importantly, 42 to 130 genes related to autoinducer 2 cell signaling were also differentially expressed, including gadAB and flgBCEGHIJLMN, as well as signaling through indole, since 17 to 26 indole-related genes were differentially expressed, including phoAER, gltBD, mtr (encodes protein for indole import), and acrEF (encodes proteins for indole export). Increased biofilm formation in the yliH and yceP mutants in LB supplemented with 0.2% glucose (LB glu) occurred through a reduction in extracellular and intracellular indole concentrations in both mutants (50- to 140-fold), and the addition of indole to the culture restored the wild-type biofilm phenotype; hence, indole represses biofilms. Additionally, both mutants regulate biofilms through quorum sensing, since deletion of either yliH or yceP increased extracellular autoinducer 2 concentrations 50-fold when grown in complex medium (most notably in the stationary phase). Both proteins are involved in motility regulation, since YliH (127 amino acids) and YceP (84 amino acids) repressed motility two to sevenfold (P ≤ 0.05) in LB, and YceP repressed motility sevenfold (P ≤ 0.05) in LB glu. Heightened motility in the yceP mutant occurred, due to increased transcription of the flagella and motility loci, including fliC, motA, and qseB (3- to 86-fold). We propose new names for these two loci: bssR for yliH and bssS for yceP, based on the phrase “regulator of biofilm through signal secretion.”

A Broad-Spectrum Antibiofilm Peptide Enhances Antibiotic Action against Bacterial Biofilms

Abstract: Biofilm-related infections account for at least 65% of all human infections, but there are no available antimicrobials that specifically target biofilms. Their elimination by available treatments is inefficient since biofilm cells are between 10- and 1,000-fold more resistant to conventional antibiotics than planktonic cells. Here we describe the synergistic interactions, with different classes of antibiotics, of a recently characterized antibiofilm peptide, 1018, to potently prevent and eradicate bacterial biofilms formed by multidrug-resistant ESKAPE (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species) pathogens. Combinations of peptide 1018 and the antibiotic ceftazidime, ciprofloxacin, imipenem, or tobramycin were synergistic in 50% of assessments and decreased by 2- to 64-fold the concentration of antibiotic required to treat biofilms formed by Pseudomonas aeruginosa, Escherichia coli, Acinetobacter baumannii, Klebsiella pneumoniae, Salmonella enterica, and methicillin-resistant Staphylococcus aureus. Furthermore, in flow cell biofilm studies, combinations of low, subinhibitory levels of the peptide (0.8 μg/ml) and ciprofloxacin (40 ng/ml) decreased dispersal and triggered cell death in mature P. aeruginosa biofilms. In addition, short-term treatments with the peptide in combination with ciprofloxacin prevented biofilm formation and reduced P. aeruginosa PA14 preexisting biofilms. PCR studies indicated that the peptide suppressed the expression of various antibiotic targets in biofilm cells. Thus, treatment with the peptide represents a novel strategy to potentiate antibiotic activity against biofilms formed by multidrug-resistant pathogens.