scholarly journals Identification of the quorum sensing molecule in pathogenic Mucorale Rhizopus arrhizus and its impact on fungal growth and biofilm formation

2021 ◽  
Vol 39 ◽  
pp. S113
Author(s):  
Mahaldeep Kaur ◽  
Rachna Singh
2002 ◽  
Vol 68 (11) ◽  
pp. 5459-5463 ◽  
Author(s):  
Gordon Ramage ◽  
Stephen P. Saville ◽  
Brian L. Wickes ◽  
José L. López-Ribot

ABSTRACT Farnesol is a quorum-sensing molecule that inhibits filamentation in Candida albicans. Both filamentation and quorum sensing are deemed to be important factors in C. albicans biofilm development. Here we examined the effect of farnesol on C. albicans biofilm formation. C. albicans adherent cell populations (after 0, 1, 2, and 4 h of adherence) and preformed biofilms (24 h) were treated with various concentrations of farnesol (0, 3, 30, and 300 μM) and incubated at 37°C for 24 h. The extent and characteristics of biofilm formation were then assessed microscopically and with a semiquantitative colorimetric technique based on the use of 2,3-bis(2-methoxy-4-nitro-5-sulfo-phenyl)-2H-tetrazolium-5-carboxanilide. The results indicated that the effect of farnesol was dependent on the concentration of this compound and the initial adherence time, and preincubation with 300 μM farnesol completely inhibited biofilm formation. Supernatant media recovered from mature biofilms inhibited the ability of planktonic C. albicans to form filaments, indicating that a morphogenetic autoregulatory compound is produced in situ in biofilms. Northern blot analysis of RNA extracted from cells in biofilms indicated that the levels of expression of HWP1, encoding a hypha-specific wall protein, were decreased in farnesol-treated biofilms compared to the levels in controls. Our results indicate that farnesol acts as a naturally occurring quorum-sensing molecule which inhibits biofilm formation, and we discuss its potential for further development and use as a novel therapeutic agent.


2018 ◽  
Author(s):  
Frederic Gaspar ◽  
Neuza Teixeira ◽  
Natalia Montero ◽  
Tamara Aleksandrzak-Piekarczyk ◽  
Renata Matos ◽  
...  

AbstractThe AI-2 i nterspecies quorum-sensing molecule is produced by the LuxS enzyme and has been ascribed a role in virulence in several bacteria. The nosocomial pathogenEnterococcus faecalisinhabits several different environments where multispecies communities are established. However, despite the presence of aluxSgene in this pathogen, its role inE. faecalispathogenesis has never been assessed. In the present work, we deleted theluxSgene from the vancomycin-resistant clinical isolateE. faecalisV583 and demonstrated the lack of AI-2 production by the mutant strain. Using microarrays and externally added (S)-4,5-dihydroxy-2,3-pentanedione we showed that AI-2 is not sensed byE. faecalisas a canonical quorum-sensing molecule and that theluxSmutation caused pleiotropic effects in gene expression, which could not be complemented by extracellularly added AI-2. These global differences in gene expression affected several gene functional roles, mainly those enrolled in metabolism and transport. Metabolic phenotypi ng of theluxSmutant, using Biolog plates, showed differences in utilization of galactose. AI-2 production by LuxS was shown to be irrelevant for some phenotypes related to the pathogenic potential ofE. faecalisnamely biofilm formation, adhesion to Caco-2 cells, resistance to oxidative stress and survival inside J-774 macrophages. However, theluxSmutant was attenuated when tested in theDrosophilaseptic injury model, as its deletion led to delayed fly death. Overall our findings show that differential gene expression related to theluxSmutation cannot be ascribed to quorum-sensing. Moreover, the role of LuxS appears to be limited to metabolism.


2015 ◽  
Vol 66 (4-6) ◽  
pp. 413-418
Author(s):  
أميرة إسماعيل عبد الحميد ◽  
سناء محمد إبراهيم زكي ◽  
علا إبراهيم أحمد ◽  
مروي سعد محمد فتحي ◽  
نانسي محمد أبو شادي

2021 ◽  
Vol 30 (1) ◽  
pp. 1-11
Author(s):  
Sunjukta Ahsan ◽  
Nur E Alam ◽  
Ahmed Salman Sirajee

The ability of E. coli to form complex surface-associated communities, called biofilms, contribute to its resistance and persistence in Urinary Tract Infection (UTI). In the present study, the ability of uropathogenic E. coli (n=30) isolated from UTI patients to form biofilm and the concentration of Azithromycin to inhibit or kill planktonic and biofilm phase bacteria were investigated. Effects of sub-Minimum Inhibitory Concentration (MIC) of Azithromycin on biofilm formation was investigated. An attempt was also taken to identify the quorum sensing molecule released by E. coli in biofilm. Among the 30 isolates, 6 (20%) were very strong, 8 (26.67%) were strong, 13 (43.33%) were moderate and 3 (10%) were weak biofilm producers. MIC and MBC (Minimum bactericidal concentration) of planktonic phase bacteria were determined and compared with MRC (Minimum regrowth concentration) and MBEC (Minimum biofilm eradication concentration) of biofilm population. MIC values ranged between 0.5 μg/ml to greater than 512 μg/ml. MBC values were measured for ten isolates and the range found was between 8-64 μg/ml. It was found that MRC values were 2-256 times greater than MIC values and MBEC values were 16-256 times greater than corresponding MBC values. After subjecting sub MIC Azithromycin levels to 10 selected isolates, 6 lost the ability to form curli fimbriae and 2 lost their capability of motility in planktonic stage, but none of this ability was lost in biofilm stage. Viable cell count of planktonic cells incubated in sub MIC Azithromycin concentration showed significant decrease of cell number whereas the number of planktonic cells without antibiotic increased significantly. In contrast, for biofilm forming cells, no change in cell number was seen with progressing time for either the presence or absence of antibiotic indicating that biofilm formation could not be inhibited by sub MIC concentrations of Azithromycin. It can be implied that Azithromycin is not the proper drug of choice for eradication of biofilm formed by E. coli. The present study failed to identify the quorum sensing molecule released by the test isolates by the method employed. Dhaka Univ. J. Biol. Sci. 30(1): 1-11, 2021 (January)


Microbiology ◽  
2020 ◽  
Vol 166 (1) ◽  
pp. 44-55 ◽  
Author(s):  
Hasan Nazik ◽  
Gabriele Sass ◽  
Shajia R. Ansari ◽  
Reyhan Ertekin ◽  
Hubertus Haas ◽  
...  

Pseudomonas aeruginosa (Pa) and Aspergillus fumigatus (Af), the commonest bacterium and fungus in compromised host airways, compete for iron (Fe). The Pseudomonas quinolone signal (PQS), a Pa quorum sensing molecule, also chelates Fe, and delivers Fe to the Pa cell membrane using Pa siderophores. In models of Af biofilm formation or preformed biofilms, PQS inhibited Af in a low Fe environment. AfΔsidA (mutant unable to produce siderophores) biofilm was more sensitive to PQS inhibition than wild-type (WT), as was planktonic AfΔsidA growth. PQS decreased WT Af growth on agar. All these inhibitory actions were reversed by Fe. The Pa siderophore pyoverdin, or Af siderophore inhibitor celastrol, act cooperatively with PQS in Af inhibition. These findings all indicate PQS inhibition is owing to Fe chelation. Remarkably, in high Fe environments, PQS enhanced Af biofilm at 1/100 to 1/2000 Fe concentration required for Fe alone to enhance. Planktonic Af growth, and on agar, Af conidiation, were also enhanced by PQS+Fe compared to Fe alone. In contrast, neither AfΔsidA biofilm, nor planktonic AfΔsidA, were enhanced by PQS-Fe compared to Fe. When Af siderophore ferricrocin (FC),+PQS, were added to AfΔsidA, Af was then boosted more than by FC alone. Moreover, FC+PQS+Fe boosted AfΔsidA more than Fe, FC, FC+Fe, PQS+FC or PQS+Fe. Thus PQS-Fe maximal stimulation requires Af siderophores. PQS inhibits Af via chelation under low Fe conditions. In a high Fe environment, PQS paradoxically stimulates Af efficiently, and this involves Af siderophores. PQS production by Pa could stimulate Af in cystic fibrosis airways, where Fe homeostasis is altered and Fe levels increase, supporting fungal growth.


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