| Literature DB >> 26843692 |
Shikha Koul1, Jyotsana Prakash1, Anjali Mishra2, Vipin Chandra Kalia1.
Abstract
Expression of certain bacterial genes only at a high bacterial cell density is termed as quorum-sensing (QS). Here bacteria use signaling molecules to communicate among themselves. QS mediated genes are generally involved in the expression of phenotypes such as bioluminescence, biofilm formation, competence, nodulation, and virulence. QS systems (QSS) vary from a single in Vibrio spp. to multiple in Pseudomonas and Sinorhizobium species. The complexity of QSS is further enhanced by the multiplicity of signals: (1) peptides, (2) acyl-homoserine lactones, (3) diketopiperazines. To counteract this pathogenic behaviour, a wide range of bioactive molecules acting as QS inhibitors (QSIs) have been elucidated. Unlike antibiotics, QSIs don't kill bacteria and act at much lower concentration than those of antibiotics. Bacterial ability to evolve resistance against multiple drugs has cautioned researchers to develop QSIs which may not generate undue pressure on bacteria to develop resistance against them. In this paper, we have discussed the implications of the diversity and multiplicity of QSS, in acting as an arsenal to withstand attack from QSIs and may use these as reservoirs to develop multi-QSI resistance.Entities:
Keywords: Antibiotics; Bioactive molecules; Drug resistance; Quorum-sensing; Quorum-sensing inhibitors
Year: 2015 PMID: 26843692 PMCID: PMC4729740 DOI: 10.1007/s12088-015-0558-0
Source DB: PubMed Journal: Indian J Microbiol ISSN: 0046-8991 Impact factor: 2.461