scholarly journals Streptococcus salivarius K12 inhibits Candida albicans aggregation, biofilm formation and dimorphism

Biofouling ◽  
2021 ◽  
pp. 1-10
Author(s):  
Munirah Mokhtar ◽  
Nurul Alia Risma Rismayuddin ◽  
Aini Syahida Mat Yassim ◽  
Hasna Ahmad ◽  
Ridhwan Abdul Wahab ◽  
...  
2020 ◽  
Vol 18 (2) ◽  
Author(s):  
Munirah Mokhtar ◽  
Alia Risma Rismayuddin ◽  
Ridhwan Abdul Wahab ◽  
Muhamad Ashraf Rostam ◽  
Mohd Hamzah Mohd Nasir ◽  
...  

Introduction:  Oral cancer is the sixth most common cancer worldwide with  Candida albicans  infection being one of the aetiological factors for the disease. Meanwhile,  Streptococcus salivarius  K12 is an oral probiotic that is beneficial to the oral cavity. The objective of the present study is to determine the effect of  S. salivarius  K12 on  C. albicans  biofilm-forming ability with the hypothesis that  S. salivarius  K12 inhibits biofilm formation of  C. albicans  Materials and method: To assess the effect of  S. salivarius  K12 on  C. albicans  biofilm formation,  S. salivarius  K12, lab strain  C. albicans  MYA-4901 and clinical isolates from oral cancer, ALC2 and ALC3 were grown in both nutrient broth (NB) and RPMI. In a mono-species biofilm, 105 of  C. albicans  cells and 106 of  S. salivarius  K12 cells were grown separately in a 96-well plate. In contrast, both microorganisms were combined for polymicrobial biofilms with similar cell numbers as in mono-species. The biofilms were incubated for 72 hours at 37°C and the media were replenished every 24 hours. Finally, the crystal violet assay was conducted, and the optical density was measured at OD620nm.  Results: Polymicrobial biofilms of  C. albicans  (MYA-4901 and ALC3) with  S. salivarius K12 when grown in NB, exhibited a decrease by 64.5 ± 25.8% and 83.7 ± 5.4%, respectively when compared to the expected biofilms which were predominated by yeast form.  Furthermore, polymicrobial biofilms of  C. albicans  (ALC2 and ALC3) with  S. salivarius  K12 showed a decrease by 62.5 ± 25.6% and 55.9 ± 17.1 %, respectively when compared to the expected biofilms when grown in RPMI that were predominated by hyphal form.  Conclusion:  S. salivarius  K12 inhibited polymicrobial biofilms formation of  C. albicans  yeast and hyphal forms, thus supported the hypothesis that  S. salivarius  K12 inhibits biofilm formation of  C. albicans.


2011 ◽  
Vol 56 (1) ◽  
pp. 148-153 ◽  
Author(s):  
Marisa H. Miceli ◽  
Stella M. Bernardo ◽  
T. S. Neil Ku ◽  
Carla Walraven ◽  
Samuel A. Lee

ABSTRACTInfections and thromboses are the most common complications associated with central venous catheters. Suggested strategies for prevention and management of these complications include the use of heparin-coated catheters, heparin locks, and antimicrobial lock therapy. However, the effects of heparin onCandida albicansbiofilms and planktonic cells have not been previously studied. Therefore, we sought to determine thein vitroeffect of a heparin sodium preparation (HP) on biofilms and planktonic cells ofC. albicans. Because HP contains two preservatives, methyl paraben (MP) and propyl paraben (PP), these compounds and heparin sodium without preservatives (Pure-H) were also tested individually. The metabolic activity of the mature biofilm after treatment was assessed using XTT [2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide] reduction and microscopy. Pure-H, MP, and PP caused up to 75, 85, and 60% reductions of metabolic activity of the mature preformedC. albicansbiofilms, respectively. Maximal efficacy against the mature biofilm was observed with HP (up to 90%) compared to the individual compounds (P< 0.0001). Pure-H, MP, and PP each inhibitedC. albicansbiofilm formation up to 90%. A complete inhibition of biofilm formation was observed with HP at 5,000 U/ml and higher. When tested against planktonic cells, each compound inhibited growth in a dose-dependent manner. These data indicated that HP, MP, PP, and Pure-H havein vitroantifungal activity againstC. albicansmature biofilms, formation of biofilms, and planktonic cells. Investigation of high-dose heparin-based strategies (e.g., heparin locks) in combination with traditional antifungal agents for the treatment and/or prevention ofC. albicansbiofilms is warranted.


Author(s):  
Gunderao Hanumantrao Kathwate ◽  
Ravikumar Bapurao Shinde ◽  
S. Mohan Karuppayil

2021 ◽  
Vol 50 (7) ◽  
pp. 2627-2638
Author(s):  
Tina P. Andrejević ◽  
Ivana Aleksic ◽  
Marta Počkaj ◽  
Jakob Kljun ◽  
Dusan Milivojevic ◽  
...  

Antifungal copper(ii) complexes with pyridine-4,5-dicarboxylate esters show the ability to inhibit the filamentation and biofilm formation of Candida albicans, and efficiently prevent the adhesion of this fungus.


2007 ◽  
Vol 6 (6) ◽  
pp. 931-939 ◽  
Author(s):  
Fang Li ◽  
Michael J. Svarovsky ◽  
Amy J. Karlsson ◽  
Joel P. Wagner ◽  
Karen Marchillo ◽  
...  

ABSTRACT Candida albicans is the leading cause of systemic fungal infections in immunocompromised humans. The ability to form biofilms on surfaces in the host or on implanted medical devices enhances C. albicans virulence, leading to antimicrobial resistance and providing a reservoir for infection. Biofilm formation is a complex multicellular process consisting of cell adhesion, cell growth, morphogenic switching between yeast form and filamentous states, and quorum sensing. Here we describe the role of the C. albicans EAP1 gene, which encodes a glycosylphosphatidylinositol-anchored, glucan-cross-linked cell wall protein, in adhesion and biofilm formation in vitro and in vivo. Deleting EAP1 reduced cell adhesion to polystyrene and epithelial cells in a gene dosage-dependent manner. Furthermore, EAP1 expression was required for C. albicans biofilm formation in an in vitro parallel plate flow chamber model and in an in vivo rat central venous catheter model. EAP1 expression was upregulated in biofilm-associated cells in vitro and in vivo. Our results illustrate an association between Eap1p-mediated adhesion and biofilm formation in vitro and in vivo.


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