Role of exopolymeric substances (EPS) in the stability of the biofilm of Thiomonas arsenivorans grown on a porous mineral support.

Biochemical methods were selected to evaluate the role of exopolymeric substances in the stability of biofilms used in bioremediation processes. Biofilms of Thiomonas arsenivorans formed on pozzolana were thus treated with pronase (protein target), lectins (Con A or PNA), calcofluor or periodic acid (polysaccharides target), DNase (DNA target), and lipase (triglycerides target). Neither protease nor DNase treatments had any effect on bacterial adhesion. Lectins and calcofluor treatments mainly affected young biofilms. Lipase treatment had a noticeable effect on biofilm stability whatever the biofilm age. Results suggest that it would be an increased resistance of mature biofilms that protects them from external attacks.

Enhancing pozzolana colonization by As(III)-oxidizing bacteria for bioremediation purposes.

The colonization of pozzolana by an As(III)-oxidizing bacterial consortium was monitored from the first hours of bacterial adhesion to 6 weeks of development under fed-batch conditions, using adapted ultrasonic dislodging and crystal-violet staining procedures to determine the biofilm adhering to the complex surfaces. The effect of temperature, arsenic concentration, and presence or absence of yeast extract (YE) on the amount of biofilm biomass and on the As(III)-oxidation were assessed to test the biofilm's resilience and optimize the colonization. Fed-batch cultures allow twice as much pozzolana colonization as that obtained under batch conditions. In addition, As(III) oxidation and the quantities of biomass under fed-batch culture conditions were the same at 14 degrees C and 25 degrees C. Whereas YE improves (+150%) bacterial adhesion during the first 2 h, its impact in the longer term appears to be less significant-biofilm formation in presence of YE after 5 weeks was no greater than biofilm formation in the absence of YE. Finally, YE involves a drastic (-70%) decrease of As(III) oxidation. Preliminary tests for drinking-water bioremediation revealed the ability of Chéni Arsenic Oxidizing 1 biofilms to remain and retain As(III) oxidation activity at low As(III) concentrations (50 microg l(-1)).

Assessment of the roles of LuxS, S-ribosyl homocysteine, and autoinducer 2 in cell attachment during biofilm formation by Listeria monocytogenes EGD-e.

LuxS is responsible for the production of autoinducer 2 (AI-2), which is involved in the quorum-sensing response of Vibrio harveyi. AI-2 is found in several other gram-negative and gram-positive bacteria and is therefore considered a good candidate for an interspecies communication signal molecule. In order to determine if this system is functional in the gastrointestinal pathogen Listeria monocytogenes EGD-e, an AI-2 bioassay was performed with culture supernatants. The results indicated that this bacterium produces AI-2 like molecules. A potential ortholog of V. harveyi luxS, lmo1288, was found by performing sequence similarity searches and complementation experiments with Escherichia coli DH5alpha, a luxS null strain. lmo1288 was found to be a functional luxS ortholog involved in AI-2 synthesis. Indeed, interruption of lmo1288 resulted in loss of the AI-2 signal. Although no significant differences were observed between Lux1 and EGD-e with regard to planktonic growth (at 10 degrees C, 15 degrees C, 25 degrees C, and 42 degrees C), swimming motility, and phospholipase and hemolytic activity, biofilm culture experiments showed that under batch conditions between 25% and 58% more Lux1 cells than EGD-e cells were attached to the surface depending on the incubation time. During biofilm growth in continuous conditions after 48 h of culture, Lux1 biofilms were 17 times denser than EGD-e biofilms. Finally, our results showed that Lux1 accumulates more S-adenosyl homocysteine (SAH) and S-ribosyl homocysteine (SRH) in culture supernatant than the parental strain accumulates and that SRH, but not SAH or AI-2, is able to modify the number of attached cells.