Interaction of Chlorhexidine with Cytoplasmic Membranes of Streptococcus mutans GS-5

Koontongkaew, Sittichai; Jitpukdeebodintra, Suwanna

doi:10.1159/000262101

Cited by 14 publications

(10 citation statements)

References 19 publications

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“…This suggests that in the zoocin A-and lauricidin-treated biofilms, the metabolic activity of S. mutans was compromised to a greater degree relative to cell death than in the chlorhexidine-treated biofilms, an effect that may relate to the mode of action of the respective compounds. Lauricidin and chlorhexidine both have the bacterial membrane as their primary site of action, however, while the positively charged chlorhexidine interacts directly with negatively charged membrane components [Koontongkaew and Jitpukdeebodintra, 1995], the neutrally charged lauricidin has been shown to also effect cytoplasmic targets including metabolism [Kabara, 1993].…”

Section: Discussionmentioning

confidence: 99%

Zoocin A and Lauricidin in Combination Reduce <i>Streptococcus mutans</i> Growth in a Multispecies Biofilm

Lester¹,

Simmonds²

2012

Caries Res

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Dental caries is the most prevalent human infection. It is a multifactorial disease in which the microbial composition of dental plaque plays a major role in the development of clinical symptoms. The bacteria most often implicated in the development of caries are that group of streptococci referred to as the mutans streptococci, in particular Streptococcus mutans and Streptococcus sobrinus. One approach to the prevention of caries is to reduce the numbers of mutans streptococci in plaque to a level insufficient to support demineralization of the tooth. In this study, zoocin A, a peptidoglycan hydrolase, combined with lauricidin, a cell membrane active lipid, was shown over a 72 h period to selectively suppress the growth of S. mutans in a triple species biofilm. Growth of the non-target species Streptococcus oralis and Actinomyces viscosus was not inhibited. In treated systems the amount of extracellular polysaccharide matrix produced was much reduced as determined by use of fluorescein isothiocyanate conjugated wheat germ agglutinin. The pH of treated biofilms remained above neutral as opposed to a value of 4.3 in untreated controls. We conclude that use of antimicrobial compounds that specifically target cariogenic bacteria should be further explored.

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Section: Discussionmentioning

confidence: 99%

Zoocin A and Lauricidin in Combination Reduce <i>Streptococcus mutans</i> Growth in a Multispecies Biofilm

Lester¹,

Simmonds²

2012

Caries Res

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“…The chlorhexidine remains on the skin, providing an antimicrobial coating that is replenished with each bathing. Chlorhexidine is amphipathic, and it likely interacts with both phospholipids and proteins on the bacterial cell surface (15,16). Its interaction with the membrane is reported to be similar to that of antimicrobial peptides (15).…”

mentioning

confidence: 99%

Chlorhexidine Induces VanA-Type Vancomycin Resistance Genes in Enterococci

Bhardwaj

Ziegler

Palmer

2016

Antimicrob Agents Chemother

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Chlorhexidine is a bisbiguanide antiseptic used for infection control. Vancomycin-resistant E. faecium (VREfm) is among the leading causes of hospital-acquired infections. VREfm may be exposed to chlorhexidine at supra-and subinhibitory concentrations as a result of chlorhexidine bathing and chlorhexidine-impregnated central venous catheter use. We used RNA sequencing to investigate how VREfm responds to chlorhexidine gluconate exposure. Among the 35 genes upregulated >10-fold after 15 min of exposure to the MIC of chlorhexidine gluconate were those encoding VanA-type vancomycin resistance (vanHAX) and those associated with reduced daptomycin susceptibility (liaXYZ). We confirmed that vanA upregulation was not strain or species specific by querying other VanA-type VRE. VanB-type genes were not induced. The vanH promoter was found to be responsive to subinhibitory chlorhexidine gluconate in VREfm, as was production of the VanX protein. Using vanH reporter experiments with Bacillus subtilis and deletion analysis in VREfm, we found that this phenomenon is VanR dependent. Deletion of vanR did not result in increased chlorhexidine susceptibility, demonstrating that vanHAX induction is not protective against chlorhexidine. As expected, VanA-type VRE is more susceptible to ceftriaxone in the presence of sub-MIC chlorhexidine. Unexpectedly, VREfm is also more susceptible to vancomycin in the presence of subinhibitory chlorhexidine, suggesting that chlorhexidine-induced gene expression changes lead to additional alterations in cell wall synthesis. We conclude that chlorhexidine induces expression of VanA-type vancomycin resistance genes and genes associated with daptomycin nonsusceptibility. Overall, our results indicate that the impacts of subinhibitory chlorhexidine exposure on hospital-associated pathogens should be further investigated in laboratory studies.

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“…Maisetta et al [20] showed that chlorhexidine might facilitate the access of human b-defensin 3 to the cytoplasmic membrane via damaging the outer bacterial membrane, which represents the main site of action. Similarly, Koontongkaew and Jitpukdeebodintra [21] found the effect of CHXD on cell membranes of Streptococcus mutans GS-5 after treating the extracted proteins for 30 min with the drug at final concentrations of 0.05% and 0.2% chlorhexidine caused selective reduction in the intensity of the membrane proteins. In addition, Kim et al [22] showed marked synergistic anti-bacterial effects of gaegurin 6 (GGN6), an animalderived cationic peptide, and its derivatives PTP6 and PTP12 with chlorhexidine on the growth of oral streptococci.…”

Section: Discussionmentioning

confidence: 84%

The Effect of Brief Exposure to Sub-Therapeutic Concentrations of Chlorhexidine Digluconate on the Susceptibility of Staphylococci to Platelet Microbicidal Protein

IvanovIuri

Гриценко

KuzminMichael

2015

Surgical Infections

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The combined data indicate that PMP exerts cooperative bactericidal effect with CHXD. The anti-staphylococcal PMP and CHXD synergistic activity in vitro demonstrated in the present study make these molecules potentially useful for preventing endovascular catheter-associated infections. Future research based on animal and human models is needed to elucidate the in vivo efficacies and toxicities and utility in clinical practice.

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Interaction of Chlorhexidine with Cytoplasmic Membranes of Streptococcus mutans GS-5

Cited by 14 publications

References 19 publications

Zoocin A and Lauricidin in Combination Reduce <i>Streptococcus mutans</i> Growth in a Multispecies Biofilm

Zoocin A and Lauricidin in Combination Reduce <i>Streptococcus mutans</i> Growth in a Multispecies Biofilm

Chlorhexidine Induces VanA-Type Vancomycin Resistance Genes in Enterococci

The Effect of Brief Exposure to Sub-Therapeutic Concentrations of Chlorhexidine Digluconate on the Susceptibility of Staphylococci to Platelet Microbicidal Protein

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