Quorum sensing in<i>Serratia</i>

Houdt, Rob Van; Givskov, Michael; Michiels, Chris W.

doi:10.1111/j.1574-6976.2007.00071.x

Cited by 177 publications

(181 citation statements)

References 184 publications

(271 reference statements)

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“…is an opportunistic pathogen and one of the ten most common causative factors of bacteremia in North America [63]. They are responsible for a variety of infections, including bacteremia, pneumonia, intravenous catheter-associated infections, osteomyelitis, endocarditis, and, rarely, endogenous and exogenous endophthalmitis [64,65]. The mortality rate from bacteremia due to Serratia spp., 6 months after infection, is 37% [66].…”

Section: Discussionmentioning

confidence: 99%

Rhamnolipids, Microbial Virulence Factors, in Alzheimer’s Disease

Andreadou

Pantazaki

Daniilidou

et al. 2017

JAD

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Abstract. Alzheimer's disease (AD) has been attributed to chronic bacterial infections. The recognition of human microbiota as a substantial contributor to health and disease is relatively recent and growing. During evolution, mammals live in a symbiotic state with myriads of microorganisms that survive at a diversity of tissue micro-surroundings. Microbes produce a plethora of secretory products [amyloids, lipopolysaccharides, virulence factors rhamnolipids (RLs), toxins, and a great number of neuroactive compounds]. The contribution of infectious microbial components to the pathophysiology of the human central nervous system including AD is considered potentially substantial, but the involvement of the RLs has never been reported. Here, RLs were isolated from serum and identified through various conventional methods including the colorimetric orcinol method, thin-layer chromatography, attenuated total reflection Fourier transform infrared (ATR-FTIR), and dot blot using antibodies against RLs. Dot blot demonstrated elevated RL levels in sera of AD patients compared to controls (p = 0.014). Moreover, ELISA showed similarly elevated RL levels in cerebrospinal fluid of both AD (0.188 versus 0.080) (p = 0.04) and mild cognitive impairment (0.188 versus 0.129) (p = 0.088) patients compared to healthy, and are wellcorrelated with the AD stages severity assessed using the Mini-Mental State Examination. These results provide conclusive evidence for the newly-reported implication of RLs in AD, adding it to the list of bacterial components, opening new avenues for AD investigation. Moreover, they strengthen and vindicate the divergence of research toward the exploration of bacterial involvement in AD generation and progression.

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Section: Discussionmentioning

confidence: 99%

Rhamnolipids, Microbial Virulence Factors, in Alzheimer’s Disease

Andreadou

Pantazaki

Daniilidou

et al. 2017

JAD

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“…In strains of S. marcescens, multicellular surface motility ('swarming') is facilitated by the QSmediated production of a surfactant (Van Houdt et al, 2007). Wild-type S. marcescens MG1 swarms over semi-solid surfaces ( (Lindum et al, 1998); Figure 3), while the disruption of the AHL synthase gene swrI significantly delays the appearance of the swarm ( (Lindum et al, 1998); Figure 3).…”

Section: Effect On Swarming In Serratia Marcescensmentioning

confidence: 99%

“…The bestcharacterized QS signals are N-acyl homoserine lactones (AHLs) (Eberhard et al, 1981;Fuqua et al, 2001). In many Gram-negative bacteria, including members of the Serratia genus, QS controls surface spreading, production of antibiotics and exoenzymes, attachment to surfaces and timing of virulence gene expression (Van Houdt et al, 2007). Production of QS signals has also been reported in cultures of coral-associated vibrios, although the role of QS in coral diseases caused by these microorganisms has not yet been established (Tait et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Signaling-mediated cross-talk modulates swarming and biofilm formation in a coral pathogen Serratia marcescens

et al. 2011

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Interactions within microbial communities associated with marine holobionts contribute importantly to the health of these symbiotic organisms formed by invertebrates, dinoflagellates and bacteria. However, mechanisms that control invertebrate-associated microbiota are not yet fully understood. Hydrophobic compounds that were isolated from surfaces of asymptomatic corals inhibited biofilm formation by the white pox pathogen Serratia marcescens PDL100, indicating that signals capable of affecting the associated microbiota are produced in situ. However, neither the origin nor structures of these signals are currently known. A functional survey of bacteria recovered from coral mucus and from cultures of the dinoflagellate Symbiodinium spp. revealed that they could alter swarming and biofilm formation in S. marcescens. As swarming and biofilm formation are inversely regulated, the ability of some native a-proteobacteria to affect both behaviors suggests that the a-proteobacterial signal(s) target a global regulatory switch controlling the behaviors in the pathogen. Isolates of Marinobacter sp. inhibited both biofilm formation and swarming in S. marcescens PDL100, without affecting growth of the coral pathogen, indicative of the production of multiple inhibitors, likely targeting lower level regulatory genes or functions. A multi-species cocktail containing these strains inhibited progression of a disease caused by S. marcescens in a model polyp Aiptasia pallida. An a-proteobacterial isolate 44B9 had a similar effect. Even though B4% of native holobiont-associated bacteria produced compounds capable of triggering responses in well-characterized N-acyl homoserine lactone (AHL) biosensors, there was no strong correlation between the production of AHL-like signals and disruption of biofilms or swarming in S. marcescens.

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“…SplI/SplR C4HSL, C6HSL, 3OC6HSL Production of nuclease, chitinase, protease and antibacterial compound; butanediol fermentation [117] Serratia proteamaculans…”

Section: Rvh1mentioning

confidence: 99%

“…SmaI/SmaR, SwrI/SwrR, SpnI/SpnR and SplI/SplR are the four homologues of the luxIR system present across Serratia species that regulates phenotypes such as swarming and sliding motility, exo-enzymes, antibiotic production, biofilm formation, butanediol fermentation (Table 3) [114][115][116][117][118].…”

Section: Serratiamentioning

confidence: 99%

Potential Emergence of Multi-quorum Sensing Inhibitor Resistant (MQSIR) Bacteria

et al. 2015

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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.

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Quorum sensing inSerratia

Cited by 177 publications

References 184 publications

Rhamnolipids, Microbial Virulence Factors, in Alzheimer’s Disease

Rhamnolipids, Microbial Virulence Factors, in Alzheimer’s Disease

Signaling-mediated cross-talk modulates swarming and biofilm formation in a coral pathogen Serratia marcescens

Potential Emergence of Multi-quorum Sensing Inhibitor Resistant (MQSIR) Bacteria

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