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Cell-to-Cell signal system in Escherichia coli Drug Resistance- a review

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Author Affiliations

  • 1Department of Microbiology, Federal University of Technology, Minna, Nigeria
  • 2Department of Microbiology, Federal University of Technology, Minna, Nigeria
  • 3Department of Biological Sciences, Niger State Polytechnic, Zungeru, Nigeria
  • 4Department of Microbiology, Federal University of Technology, Minna, Nigeria
  • 5Department of Biological Sciences, Federal Polytechnic, Bida, Nigeria
  • 6Department of Microbiology, Federal University of Technology, Minna, Nigeria

Int. Res. J. Environment Sci., Volume 6, Issue (8), Pages 51-59, August,22 (2017)

Abstract

The term drug resistance refers to the ability of microorganisms to resist a drug that once stalled or killed them. Drug resistance in Escherichia coli may occur via production and elaboration of beta-lactamases, impermeability by simple closure of porin channels or lipopolysaccharide expression and removal of the anti-microbial compounds from the bacterial cell through specific and/or general efflux pumps. Drug resistance may be innate or adaptive. Cell-to-cell signal system (quorum sensing, QS) is an adaptive type of drug resistance, which depends on secreted signal molecules, to initiate response synchronized across bacterial population. The signaling molecules is similar to hormones present in higher animals. Mechanisms involved in QS systems include signals production, signals accumulation, and signals detection. In quorum sensing mechanisms, E. coli secretes chemical signal molecules during its exponential growth phase. The molecule known as autoinducers (Al-2) or pheromones is mediated by luxS gene. When a certain concentration of autoinducers is obtained, known as the threshold concentration, its presence is identified and lead to the initiation of the signal cascade. The consequence of this signal cascade may include changes of target gene expression, such as drug resistance. Factors affecting cell-to-cell signal systems are temperature, salinity, pressure, and pH. Bacteria may also be more resistant to antibiotics when they work together as a group via QS mechanism. Interfering with quorum sensing is a strategy that may be used to control bacterial virulence and antibiotic resistance. Control of QS in E. coli drug resistance include the use of AI-2 synthase inhibitors, modification of AI-2, the use AI-2 analogs, antagonism for LuxR-family receptor, signal synthesis inhibition, production of degradation enzymes and signal trapping.

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