Inhibition of quorum sensing regulated biofilm formation in Serratia marcescens causing nosocomial infections

2012 ◽  
Vol 22 (9) ◽  
pp. 3089-3094 ◽  
Author(s):  
Dhamodharan Bakkiyaraj ◽  
Chandran Sivasankar ◽  
Shunmugiah Karutha Pandian
2018 ◽  
Vol 15 (3) ◽  
pp. 661-670 ◽  
Author(s):  
Kirti Marathe ◽  
Sunita Bundale ◽  
Nandita Nashikkar ◽  
Avinash Upadhyay

Quorum sensing (QS) is a bacterial cell density dependent mode of communication involved in regulation of virulence in pathogens including biofilm formation. Accordingly, curbing QS might prove to be an anti-virulence approach of controlling nosocomial infections caused by multi drug resistant bacteria. The report presented here documents the QS inhibitory properties of linoleic acid against Proteus mirabilis and Serratia marcescens known to cause nosocomial infections. Urease assay, prodigiosin assay, protease assay, biofilm formation assay and growth curve analysis were performed to investigate the effectiveness of linoleic acid in controlling virulence of P. mirabilis and S. marcescens. 2.5mM linoleic acid reduced the urease activity and biofilm formation to 42.11% and 11.11% respectively in P. mirabilis; and prodigiosin synthesis, protease activity and biofilm formation to 0%, 65.91% and 33.33% correspondingly in S. marcescens. Therefore, analysis of QS inhibitory behaviour of linoleic acid substantiates its use as a plausible drug for anti-virulence therapy without subjecting the bacteria to discerning force of antibiotics.


2007 ◽  
Vol 73 (20) ◽  
pp. 6339-6344 ◽  
Author(s):  
Tomohiro Morohoshi ◽  
Toshitaka Shiono ◽  
Kiyomi Takidouchi ◽  
Masashi Kato ◽  
Norihiro Kato ◽  
...  

ABSTRACT Quorum sensing is a regulatory system for controlling gene expression in response to increasing cell density. N-Acylhomoserine lactone (AHL) is produced by gram-negative bacteria, which use it as a quorum-sensing signal molecule. Serratia marcescens is a gram-negative opportunistic pathogen which is responsible for an increasing number of serious nosocomial infections. S. marcescens AS-1 produces N-hexanoyl homoserine lactone (C6-HSL) and N-(3-oxohexanoyl) homoserine lactone and regulates prodigiosin production, swarming motility, and biofilm formation by AHL-mediated quorum sensing. We synthesized a series of N-acyl cyclopentylamides with acyl chain lengths ranging from 4 to 12 and estimated their inhibitory effects on prodigiosin production in AS-1. One of these molecules, N-nonanoyl-cyclopentylamide (C9-CPA), had a strong inhibitory effect on prodigiosin production. C9-CPA also inhibited the swarming motility and biofilm formation of AS-1. A competition assay revealed that C9-CPA was able to inhibit quorum sensing at four times the concentration of exogenous C6-HSL and was more effective than the previously reported halogenated furanone. Our results demonstrated that C9-CPA was an effective quorum-sensing inhibitor for S. marcescens AS-1.


2015 ◽  
Vol 81 (10) ◽  
pp. 3306-3315 ◽  
Author(s):  
Sara Remuzgo-Martínez ◽  
María Lázaro-Díez ◽  
Celia Mayer ◽  
Maitane Aranzamendi-Zaldumbide ◽  
Daniel Padilla ◽  
...  

ABSTRACTSerratiaspp. are opportunistic human pathogens responsible for an increasing number of nosocomial infections. However, little is known about the virulence factors and regulatory circuits that may enhance the establishment and long-term survival ofSerratia liquefaciensin the hospital environment. In this study, two reporter strains,Chromobacterium violaceumCV026 and VIR24, and high-resolution triple-quadrupole liquid chromatography–mass spectrometry (LC-MS) were used to detect and to quantifyN-acyl-homoserine lactone (AHL) quorum-sensing signals in 20S. liquefaciensstrains isolated from clinical samples. Only four of the strains produced sufficient amounts of AHLs to activate the sensors. Investigation of two of the positive strains by high-performance liquid chromatography (HPLC)-MS confirmed the presence of significant amounts of short-acyl-chain AHLs (N-butyryl-l-homoserine lactone [C4-HSL] andN-hexanoyl-l-homoserine lactone [C6-HSL]) in both strains, which exhibited a complex and strain-specific signal profile that included minor amounts of other short-acyl-chain AHLs (N-octanoyl-l-homoserine lactone [C8-HSL] andN-3-oxohexanoyl-l-homoserine lactone [OC6-HSL]) and long-acyl-chain (C10, C12, and C14) AHLs. No correlation between biofilm formation and the production of large amounts of AHLs could be established. Fimbria-like structures were observed by transmission electron microscopy, and the presence of the type 1 fimbrial adhesin genefimHin all strains was confirmed by PCR. The ability ofS. liquefaciensto adhere to abiotic surfaces and to form biofilms likely contributes to its persistence in the hospital environment, increasing the probability of causing nosocomial infections. Therefore, a better understanding of the adherence properties of this species will provide greater insights into the diseases it causes.


Author(s):  
Zahra Fekrirad ◽  
Basira Gattali ◽  
Nasim Kashef

Background and Objectives: Serratia marcescens has emerged as a nosocomial pathogen responsible for human infections, where antibiotic resistance further complicates the treatments. In S. marcescens, biofilm formation and virulence factor production are controlled via quorum sensing (QS) system. QS is a signaling system that enables gene regulation to control diverse physiological functions in bacteria. Essential oils have shown to be potential in diminishing the pathogenicity and virulence of drug-resistant bacteria. This study was performed to determine whether eugenol would affect QS system, biofilm formation and virulence factor production of S. marcescens. Materials and Methods: Biofilm formation, extracellular virulence factor production (hemolysin and protease), swarming motility and pigment formation of S. marcescens ATCC 13880 and S. marcescens Sm2 were assessed after eugenol exposure at 1.25 and 2.5 µg/ml concentrations. The expression of genes involved in motility (flhD), attachment (fimC), biofilm formation (bsmB, bsmA), and QS regulatory (swrR) were also evaluated. Results: Eugenol treatment at 1.25 and 2.5 µg/ml concentrations caused a significant reduction in biofilm formation. The pigment, hemolysin and protease production of two studied S. marcescens strains, also reduced significantly by eugenol treatments (p<0.05). The bsmA, bsmB, flhD and fimC genes were down-regulated after eugenol treatment. The swrR gene expression was also reduced significantly by eugenol in both S. marcescens strains (p<0.05). Conclusion: Eugenol inhibited quorum sensing-regulated functions of two studied S. marcescens strains.


Biofouling ◽  
2021 ◽  
Vol 37 (2) ◽  
pp. 145-160
Author(s):  
Huai-Zhi Luo ◽  
Jin-Wei Zhou ◽  
Bing Sun ◽  
Huan Jiang ◽  
Shi Tang ◽  
...  

2005 ◽  
Vol 187 (10) ◽  
pp. 3477-3485 ◽  
Author(s):  
S. A. Rice ◽  
K. S. Koh ◽  
S. Y. Queck ◽  
M. Labbate ◽  
K. W. Lam ◽  
...  

ABSTRACT We describe here a role for quorum sensing in the detachment, or sloughing, of Serratia marcescens filamentous biofilms, and we show that nutrient conditions affect the biofilm morphotype. Under reduced carbon or nitrogen conditions, S. marcescens formed a classical biofilm consisting of microcolonies. The filamentous biofilm could be converted to a microcolony-type biofilm by switching the medium after establishment of the biofilm. Similarly, when initially grown as a microcolony biofilm, S. marcescens could be converted back to a filamentous biofilm by increasing the nutrient composition. Under high-nutrient conditions, an N-acyl homoserine lactone quorum-sensing mutant formed biofilms that were indistinguishable from the wild-type biofilms. Similarly, other quorum-sensing-dependent behaviors, such as swarming motility, could be rendered quorum sensing independent by manipulating the growth medium. Quorum sensing was also found to be involved in the sloughing of the filamentous biofilm. The biofilm formed by the bacterium consistently sloughed from the substratum after approximately 75 to 80 h of development. The quorum-sensing mutant, when supplemented with exogenous signal, formed a wild-type filamentous biofilm and sloughed at the same time as the wild type, and this was independent of surfactant production. When we removed the signal from the quorum-sensing mutant prior to the time of sloughing, the biofilm did not undergo significant detachment. Together, the data suggest that biofilm formation by S. marcescens is a dynamic process that is controlled by both nutrient cues and the quorum-sensing system.


2013 ◽  
Vol 58 (3) ◽  
pp. 1802-1805 ◽  
Author(s):  
Jeng Yeong Chow ◽  
Yuanyong Yang ◽  
Song Buck Tay ◽  
Kim Lee Chua ◽  
Wen Shan Yew

ABSTRACTAcinetobacter baumanniiis a major human pathogen associated with multidrug-resistant nosocomial infections; its virulence is attributed to quorum-sensing-mediated biofilm formation, and disruption of biofilm formation is an attractive antivirulence strategy. Here, we report the first successful demonstration of biofilm disruption in a clinical isolate ofA. baumanniiS1, using a quorum-quenching lactonase obtained by directed evolution; this engineered lactonase significantly reduced the biomass ofA. baumannii-associated biofilms, demonstrating the utility of this antivirulence strategy.


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