Cytotoxic effects of the lipopolysaccharide from Pseudomonas fluorescens on neurons and glial cells

Picot, Laurent; Chevalier, Sylvie; Mezghani-Abdelmoula, Sana; Merieau, Annabelle; Lesouhaitier, Olivier; Leroux, Philippe; Cazin, L.; Orange, Nicole; Feuilloley, Marc

doi:10.1016/s0882-4010(03)00092-5

Cited by 28 publications

(42 citation statements)

References 30 publications

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“…LPS exerts strong neurodegeneration in substantia nigra and midbrain dopaminergic neurons (10)(11)(12) as well as in hippocampal (13) and cortical neurons (14). The possibility that LPS may cause neuronal cell death also in the enteric nervous system (ENS) has not been explored.…”

Section: Exposure Of Lps To Neurons In the Central Nervous System Indmentioning

confidence: 99%

Lipopolysaccharide Induces Cell Death in Cultured Porcine Myenteric Neurons

2005

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Section: Exposure Of Lps To Neurons In the Central Nervous System Indmentioning

confidence: 99%

Lipopolysaccharide Induces Cell Death in Cultured Porcine Myenteric Neurons

2005

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“…Primary culture of glial cells was achieved as previously described (53). The Caco-2/TC7 clonal cell line, derived from parental Caco-2 cells, was kindly provided by A. Servin (INSERM, UMR-S756, Châtenay-Malabry, France) at passage 23 and was used between passages 25 and 35.…”

mentioning

confidence: 99%

“…The cytotoxic potential of P. aeruginosa strains was determined by measurement of lactate dehydrogenase (LDH) release by eukaryotic cells upon cytoplasmic membrane destabilization. LDH is a stable cytosolic enzyme, the release of which is considered an indicator of necrosis (53). Confluent Caco-2/TC7 and glial cells were infected with 10 8 CFU/ml and 10 6 CFU/ml of the three strains, respectively, for 14 h. The amount of LDH released by eukaryotic cells was determined using the Cytotox 96 enzymatic assay (Promega, Charbonnières, France), as previously described (53).…”

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confidence: 99%

Full Virulence of Pseudomonas aeruginosa Requires OprF

et al. 2011

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OprF is a general outer membrane porin of Pseudomonas aeruginosa, a well-known human opportunistic pathogen associated with severe hospital-acquired sepsis and chronic lung infections of cystic fibrosis patients. A multiphenotypic approach, based on the comparative study of a wild-type strain of P. aeruginosa, its isogenic oprF mutant, and an oprF-complemented strain, showed that OprF is required for P. aeruginosa virulence. The absence of OprF results in impaired adhesion to animal cells, secretion of ExoT and ExoS toxins through the type III secretion system (T3SS), and production of the quorum-sensing-dependent virulence factors pyocyanin, elastase, lectin PA-1L, and exotoxin A. Accordingly, in the oprF mutant, production of the signal molecules N-(3-oxododecanoyl)-L-homoserine lactone and N-butanoyl-L-homoserine lactone was found to be reduced and delayed, respectively. Pseudomonas quinolone signal (PQS) production was decreased, while its precursor, 4-hydroxy-2-heptylquinoline (HHQ), accumulated in the cells. Taken together, these results show the involvement of OprF in P. aeruginosa virulence, at least partly through modulation of the quorum-sensing network. This is the first study showing a link between OprF, PQS synthesis, T3SS, and virulence factor production, providing novel insights into virulence expression.

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“…The bacterial viability and density, and the absence of contamination were controlled by plating. Glial cells were incubated for 4 h with P. aeruginosa and glial cell death was monitored using the lactate dehydrogenase (LDH) assay release as described previously (Picot et al, 2003(Picot et al, , 2004 using the Cytotox 96 Enzymic Assay (Promega). Controls realized using bacteria alone showed that in our experimental conditions P. aeruginosa PAO1 does not produce molecules that interfere with this assay.…”

Section: Methodsmentioning

confidence: 99%

Gamma-aminobutyric acid acts as a specific virulence regulator in Pseudomonas aeruginosa

et al. 2013

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Gamma-aminobutyric acid (GABA) is widespread in the environment and can be used by animal and plants as a communication molecule. Pseudomonas species, in particular fluorescent ones, synthesize GABA and express GABA-binding proteins. In this study, we investigated the effects of GABA on the virulence of Pseudomonas aeruginosa. While exposure to GABA (10 mM) did not modify either the growth kinetics or the motility of the bacterium, its cytotoxicity and virulence were strongly increased. The Caenorhabditis elegans 'fast killing test' model revealed that GABA acts essentially through an increase in diffusible toxin(s). GABA also modulates the biofilm formation activity and adhesion properties of PAO1. GABA has no effect on cell surface polarity, biosurfactant secretion or on the lipopolysaccharide structure. The production of several exoenzymes, pyoverdin and exotoxin A is not modified by GABA but we observed an increase in cyanogenesis which, by itself, could explain the effect of GABA on P. aeruginosa virulence. This mechanism appears to be regulated by quorum sensing. A proteomic analysis revealed that the effect of GABA on cyanogenesis is correlated with a reduction of oxygen accessibility and an over-expression of oxygen-scavenging proteins. GABA also promotes specific changes in the expression of thermostable and unstable elongation factors Tuf/Ts involved in the interaction of the bacterium with the host proteins. Taken together, these results suggest that GABA is a physiological regulator of P. aeruginosa virulence.

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Cytotoxic effects of the lipopolysaccharide from Pseudomonas fluorescens on neurons and glial cells

Cited by 28 publications

References 30 publications

Lipopolysaccharide Induces Cell Death in Cultured Porcine Myenteric Neurons

Lipopolysaccharide Induces Cell Death in Cultured Porcine Myenteric Neurons

Full Virulence of Pseudomonas aeruginosa Requires OprF

Gamma-aminobutyric acid acts as a specific virulence regulator in Pseudomonas aeruginosa

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