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High Glucose Concentration Promotes Vancomycin-Enhanced Biofilm Formation of Vancomycin-Non-Susceptible Staphylococcus aureus in Diabetic Mice.

Hsu CY, Shu JC, Lin MH, Chong KY, Chen CC, Wen SM, Hsieh YT, Liao WT - PLoS ONE (2015)

Bottom Line: To address this question, the diabetic mouse model infected by vancomycin-resistant S. aureus (VRSA) was used under vancomycin treatment.A 10- and 1000-fold increase in biofilm-bound bacterial colony forming units was observed in samples from diabetic mice without and with vancomycin treatment, respectively, compared to healthy mice.By contrast, in the absence of glucose vancomycin reduced propensity to form biofilms in vitro through the increased production of proteases and DNases from VRSA.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Biotechnology and Laboratory Science, College of Medicine, Chang Gung University, No. 259, Wenhua 1st Road, Guishan, Taoyuan 333, Taiwan.

ABSTRACT
We previously demonstrated that vancomycin treatment increased acquisition of eDNA and enhanced biofilm formation of drug-resistant Staphylococcus aureus through a cidA-mediated autolysis mechanism. Recently we found that such enhancement became more significant under a higher glucose concentration in vitro. We propose that besides improper antibiotic treatment, increased glucose concentration environment in diabetic animals may further enhance biofilm formation of drug-resistant S. aureus. To address this question, the diabetic mouse model infected by vancomycin-resistant S. aureus (VRSA) was used under vancomycin treatment. The capacity to form biofilms was evaluated through a catheter-associated biofilm assay. A 10- and 1000-fold increase in biofilm-bound bacterial colony forming units was observed in samples from diabetic mice without and with vancomycin treatment, respectively, compared to healthy mice. By contrast, in the absence of glucose vancomycin reduced propensity to form biofilms in vitro through the increased production of proteases and DNases from VRSA. Our study highlights the potentially important role of increased glucose concentration in enhancing biofilm formation in vancomycin-treated diabetic mice infected by drug-resistant S. aureus.

No MeSH data available.


Related in: MedlinePlus

Bacterial autolysis triggered by vancomycin plays an important role in the enhancement of biofilm formation.Determination of the number of viable biofilm-bound bacteria in subcutaneous catheters removed from healthy/diabetic mice (A) infected with VRSA strain SJC1200 (also chloramphenicol resistance) upon chloramphenicol (Cm) treatment or (B) infected with cidA  mutant SJC1201 (autolysis deficient VRSA) upon vancomycin treatment. Six mice were used in each group.
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pone.0134852.g003: Bacterial autolysis triggered by vancomycin plays an important role in the enhancement of biofilm formation.Determination of the number of viable biofilm-bound bacteria in subcutaneous catheters removed from healthy/diabetic mice (A) infected with VRSA strain SJC1200 (also chloramphenicol resistance) upon chloramphenicol (Cm) treatment or (B) infected with cidA mutant SJC1201 (autolysis deficient VRSA) upon vancomycin treatment. Six mice were used in each group.

Mentions: We previously demonstrated that cell wall-active antibiotics but protein-suppressing agents triggered the cidA-mediated autolysis of S. aureus, leading to the enhancement of biofilm formation in vitro. Such enhancement was blocked when a cidA knockout VRSA strain SJC1201 was used [5]. Because pG1546 in SJC1200 also carries a chloramphenicol resistance cassette, vancomycin treatment was replaced by chloramphenicol, as described in the methods section. The results shown in Fig 3A indicate that chloramphenicol treatment for SJC1200 slightly reduced biofilm formation in healthy mice, but the reduction was significant (P < 0.0001) in diabetic mice. In addition, a similar level of biofilm-bound CFUs was observed when healthy/diabetic mice were infected by SJC1201 with/without vancomycin treatment (Fig 3B). The infected chloramphenicol susceptible strain, ATCC 12598, was efficaciously cleared in mice with the drug concentration used in this experiment (data not shown). As a result, release of eDNA triggered by cell wall-active antibiotics played a role in the enhancement of biofilm formation of S. aureus in diabetic mice.


High Glucose Concentration Promotes Vancomycin-Enhanced Biofilm Formation of Vancomycin-Non-Susceptible Staphylococcus aureus in Diabetic Mice.

Hsu CY, Shu JC, Lin MH, Chong KY, Chen CC, Wen SM, Hsieh YT, Liao WT - PLoS ONE (2015)

Bacterial autolysis triggered by vancomycin plays an important role in the enhancement of biofilm formation.Determination of the number of viable biofilm-bound bacteria in subcutaneous catheters removed from healthy/diabetic mice (A) infected with VRSA strain SJC1200 (also chloramphenicol resistance) upon chloramphenicol (Cm) treatment or (B) infected with cidA  mutant SJC1201 (autolysis deficient VRSA) upon vancomycin treatment. Six mice were used in each group.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4526670&req=5

pone.0134852.g003: Bacterial autolysis triggered by vancomycin plays an important role in the enhancement of biofilm formation.Determination of the number of viable biofilm-bound bacteria in subcutaneous catheters removed from healthy/diabetic mice (A) infected with VRSA strain SJC1200 (also chloramphenicol resistance) upon chloramphenicol (Cm) treatment or (B) infected with cidA mutant SJC1201 (autolysis deficient VRSA) upon vancomycin treatment. Six mice were used in each group.
Mentions: We previously demonstrated that cell wall-active antibiotics but protein-suppressing agents triggered the cidA-mediated autolysis of S. aureus, leading to the enhancement of biofilm formation in vitro. Such enhancement was blocked when a cidA knockout VRSA strain SJC1201 was used [5]. Because pG1546 in SJC1200 also carries a chloramphenicol resistance cassette, vancomycin treatment was replaced by chloramphenicol, as described in the methods section. The results shown in Fig 3A indicate that chloramphenicol treatment for SJC1200 slightly reduced biofilm formation in healthy mice, but the reduction was significant (P < 0.0001) in diabetic mice. In addition, a similar level of biofilm-bound CFUs was observed when healthy/diabetic mice were infected by SJC1201 with/without vancomycin treatment (Fig 3B). The infected chloramphenicol susceptible strain, ATCC 12598, was efficaciously cleared in mice with the drug concentration used in this experiment (data not shown). As a result, release of eDNA triggered by cell wall-active antibiotics played a role in the enhancement of biofilm formation of S. aureus in diabetic mice.

Bottom Line: To address this question, the diabetic mouse model infected by vancomycin-resistant S. aureus (VRSA) was used under vancomycin treatment.A 10- and 1000-fold increase in biofilm-bound bacterial colony forming units was observed in samples from diabetic mice without and with vancomycin treatment, respectively, compared to healthy mice.By contrast, in the absence of glucose vancomycin reduced propensity to form biofilms in vitro through the increased production of proteases and DNases from VRSA.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Biotechnology and Laboratory Science, College of Medicine, Chang Gung University, No. 259, Wenhua 1st Road, Guishan, Taoyuan 333, Taiwan.

ABSTRACT
We previously demonstrated that vancomycin treatment increased acquisition of eDNA and enhanced biofilm formation of drug-resistant Staphylococcus aureus through a cidA-mediated autolysis mechanism. Recently we found that such enhancement became more significant under a higher glucose concentration in vitro. We propose that besides improper antibiotic treatment, increased glucose concentration environment in diabetic animals may further enhance biofilm formation of drug-resistant S. aureus. To address this question, the diabetic mouse model infected by vancomycin-resistant S. aureus (VRSA) was used under vancomycin treatment. The capacity to form biofilms was evaluated through a catheter-associated biofilm assay. A 10- and 1000-fold increase in biofilm-bound bacterial colony forming units was observed in samples from diabetic mice without and with vancomycin treatment, respectively, compared to healthy mice. By contrast, in the absence of glucose vancomycin reduced propensity to form biofilms in vitro through the increased production of proteases and DNases from VRSA. Our study highlights the potentially important role of increased glucose concentration in enhancing biofilm formation in vancomycin-treated diabetic mice infected by drug-resistant S. aureus.

No MeSH data available.


Related in: MedlinePlus