Cell-to-Cell signal system in Escherichia coli drug resistance- a review

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 closure of porin channels or lipopolysaccharide expr cell through specific and/or general efflux pumps. Drug resistance may be innate or adaptive. Cell (quorum sensing, QS) is an adaptive type of drug resistance, whic synchronized across bacterial population. The signaling molecules is similar to hormones present in higher animals. Mechanisms involved in QS systems include signals production, signals accumulat 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 auto 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 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 inhibitors, modification of AI-2, the use AI production of degradation enzymes and signal trapping.