Abstract
Acinetobacter baumannii is an opportunistic nosocomial pathogen that causes severe infections especially in patients with compromised immune systems. Many Gram-negative pathogens regulate the expression of their virulence factors through cell density dependent N-acyl homoserine lactone (AHL)-mediated quorum-sensing (QS) system. A. baumannii has one quorum-sensing system which involves AbaR receptor protein that forms complex with AbaI (autoinducer synthase)-generated N-(3-hydroxydodecanoyl)-L-homoserine lactone (3-OH-C12 HSL) that regulates virulence factors, namely, biofilm formation and surface motility. Survival of A. baumannii against oxidative stress is also facilitated by QS-mediated expression of antioxidant enzymes, catalase and SOD. Phylogenetic analysis showed that A. baumannii may have acquired its QS genes from Halothiobacillus neapolitanus despite being closely related to Burkholderia ambifaria. A. baumannii shares its sites of infections in patients with Pseudomonas aeruginosa, another Gram-negative pathogen exhibiting QS. Both these pathogens show two-way AHL-mediated interspecies interactions. Such interspecies interactions could bear serious implications on severity and treatment of disease. In the present era of increasing multidrug resistance, alternative therapies like inhibition of quorum sensing seem attractive to control infections caused by A. baumannii.
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Bhargava, N., Sharma, P., Capalash, N. (2015). Quorum Sensing in Acinetobacter baumannii . In: Kalia, V. (eds) Quorum Sensing vs Quorum Quenching: A Battle with No End in Sight. Springer, New Delhi. https://doi.org/10.1007/978-81-322-1982-8_10
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