Siphonocholin isolated from red sea sponge Siphonochalina siphonella attenuates quorum sensing controlled virulence and biofilm formation

Alam, Perwez; Alqahtani, Ali S.; Husain, Fohad Mabood; Rehman, Tabish; Alajmi, Mohamed F.; Noman, Omar M.; Gamal, Ali A. El; Al-Massarani, Shaza M.; Khan, Mohammad Saeed

doi:10.1016/j.jsps.2020.09.002

Cited by 19 publications

(22 citation statements)

References 47 publications

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“…Other studies gave evidence for the potential of some biological extracts or natural products to inhibit biofilm formation and QS. Siphonocholin (Syph-1), a marine steroid isolated from Siphonochalina siphonella , at sub-MICs inhibits the biofilm and pellicle formation in A. baumannii , probably due to anti-QS activity, and reduces EPS production and swarming motility [ 146 ]. In addition, the activity-guided by the partially purified fraction F1 derived from Glycyrrhiza glabra leads to a significant reduction in QS-mediated virulence of A. baumannii by downregulating the expression of the autoinducer synthase gene, abaI , and consequently reducing the production of 3-OH-C12-HSL [ 147 ].…”

Section: Prevention and Treatment Strategies Against A Baumannii Biofilmmentioning

confidence: 99%

Gram-Negative Bacteria Holding Together in a Biofilm: The Acinetobacter baumannii Way

et al. 2021

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Bacterial biofilms are a serious public-health problem worldwide. In recent years, the rates of antibiotic-resistant Gram-negative bacteria associated with biofilm-forming activity have increased worrisomely, particularly among healthcare-associated pathogens. Acinetobacter baumannii is a critically opportunistic pathogen, due to the high rates of antibiotic resistant strains causing healthcare-acquired infections (HAIs). The clinical isolates of A. baumannii can form biofilms on both biotic and abiotic surfaces; hospital settings and medical devices are the ideal environments for A. baumannii biofilms, thereby representing the main source of patient infections. However, the paucity of therapeutic options poses major concerns for human health infections caused by A. baumannii strains. The increasing number of multidrug-resistant A. baumannii biofilm-forming isolates in association with the limited number of biofilm-eradicating treatments intensify the need for effective antibiofilm approaches. This review discusses the mechanisms used by this opportunistic pathogen to form biofilms, describes their clinical impact, and summarizes the current and emerging treatment options available, both to prevent their formation and to disrupt preformed A. baumannii biofilms.

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Section: Prevention and Treatment Strategies Against A Baumannii Biofilmmentioning

confidence: 99%

Gram-Negative Bacteria Holding Together in a Biofilm: The Acinetobacter baumannii Way

et al. 2021

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“…In addition, there is evidence that some biological extracts or natural products may have the potential to inhibit biofilm formation and QS. The latest study found that a marine steroid Siphonocholin (Syph-1) isolated from siphonella can inhibit the biofilm and pellicle formation in A. baumannii and has anti-QS properties ( Alam et al, 2020 ). Further, detailed in vivo toxicological studies are needed for the potential target of Syph-1 as a therapeutic agent.…”

Section: Quorum Sensing Inhibition In Acinetobacter Baumannmentioning

confidence: 99%

Quorum Sensing Inhibition or Quenching in Acinetobacter baumannii: The Novel Therapeutic Strategies for New Drug Development

Zhong¹,

2021

Front. Microbiol.

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Acinetobacter baumannii is a Gram-negative opportunistic nosocomial pathogen, which can cause ventilator-related and blood infection in critically ill patients. The resistance of A. baumannii clinical isolates to common antimicrobials and their tolerance to desiccation have emerged as a serious problem to public health. In the process of pathogenesis, bacteria release signals, which regulate virulence and pathogenicity-related genes. Such bacteria coordinate their virulent behavior in a cell density-dependent phenomenon called quorum sensing (QS). In contrast, the two main approaches of QS interference, quorum sensing inhibitors (QSIs) and quorum quenching (QQ) enzymes, have been developed to reduce the virulence of bacteria, thus reducing the pressure to produce bacterial drug resistance. Therefore, QSIs or QQ enzymes, which interfere with these processes, might potentially inhibit bacterial QS and ultimately biofilm formation. In this review, we aim to describe the state-of-art in the QS process in A. baumannii and elaborate on the use of QSIs or QQ enzymes as antimicrobial drugs in various potential sites of the QS pathway.

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“…Escober et al demonstrated that the nuclear factor-kappa B inhibitor N-[3,5-Bis(trifluoromethyl) phenyl]-5-chloro-2-hydroxybenzamide at sub-MIC of 0.0313 μg/mL can inhibit the initial cell attachment and biofilm formation of vancomycin-resistant S. aureus strain VRS1 in a dose-dependent manner [68] . The sub-MICs of other antimicrobial compounds, such as N-nonyloxypentyl-L-DNJ, N4-benzyl-N-2-phenylquinazoline-2,4-diamine, terpenoid (+)-nootkatone, chitosan, marine steroid siphonocholin, zinc oxide, and silver nanoparticles, are found to be able to inhibit the biofilm formation of diverse S. aureus strains [43] , [46] , [69] , [70] , [71] , [89] .…”

Section: Effects Of Sub-mics Of Antibiotics On S Aureus Biofilm Formationmentioning

confidence: 99%

Virulence alterations in staphylococcus aureus upon treatment with the sub-inhibitory concentrations of antibiotics

Chen

Zhou

Huang

et al. 2021

Journal of Advanced Research

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Siphonocholin isolated from red sea sponge Siphonochalina siphonella attenuates quorum sensing controlled virulence and biofilm formation

Cited by 19 publications

References 47 publications

Gram-Negative Bacteria Holding Together in a Biofilm: The Acinetobacter baumannii Way

Gram-Negative Bacteria Holding Together in a Biofilm: The Acinetobacter baumannii Way

Quorum Sensing Inhibition or Quenching in Acinetobacter baumannii: The Novel Therapeutic Strategies for New Drug Development

Virulence alterations in staphylococcus aureus upon treatment with the sub-inhibitory concentrations of antibiotics

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