Recent perspectives on the molecular basis of biofilm formation by Pseudomonas aeruginosa and approaches for treatment and biofilm dispersal
Language English Country United States Media print-electronic
Document type Journal Article, Review
PubMed
29352409
DOI
10.1007/s12223-018-0585-4
PII: 10.1007/s12223-018-0585-4
Knihovny.cz E-resources
- Keywords
- Alginate, Biofilm dispersal, Biofilms, EPS, Gac/Rsm pathway, Pel, Pseudomonas aeruginosa, Psl, Quorum-sensing pathway, Treatment advancement, c-di-GMP signalling pathway,
- MeSH
- Anti-Bacterial Agents pharmacology MeSH
- Drug Resistance, Bacterial MeSH
- Polysaccharides, Bacterial chemistry MeSH
- Biofilms drug effects MeSH
- Models, Biological MeSH
- Humans MeSH
- Pseudomonas aeruginosa drug effects genetics growth & development physiology MeSH
- Quorum Sensing MeSH
- Gene Expression Regulation, Bacterial MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
- Names of Substances
- Anti-Bacterial Agents MeSH
- Polysaccharides, Bacterial MeSH
Pseudomonas aeruginosa, a Gram-negative, rod-shaped bacterium causes widespread diseases in humans. This bacterium is frequently related to nosocomial infections such as pneumonia, urinary tract infections (UTIs) and bacteriaemia especially in immunocompromised patients. The current review focuses on the recent perspectives on biofilms formation by these bacteria. Biofilms are communities of microorganisms in which cells stick to each other and often adhere to a surface. These adherent cells are usually embedded within a self-produced matrix of extracellular polymeric substance (EPS). Pel, psl and alg operons present in P. aeruginosa are responsible for the biosynthesis of extracellular polysaccharide which plays an important role in cell surface interactions during biofilm formation. Recent studies suggested that cAMP signalling pathway, quorum-sensing pathway, Gac/Rsm pathway and c-di-GMP signalling pathway are the main mechanism that leads to the biofilm formation. Understanding the bacterial virulence depends on a number of cell-associated and extracellular factors and is very essential for the development of potential drug targets. Thus, the review focuses on the major genes involved in the biofilm formation, the state of art update on the biofilm treatment and the dispersal approaches such as targeting adhesion and maturation, targeting virulence factors and other strategies such as small molecule-based inhibitors, phytochemicals, bacteriophage therapy, photodynamic therapy, antimicrobial peptides and natural therapies and vaccines to curtail the biofilm formation by P. aeruginosa.
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