The effects of d-Tyrosine combined with amikacin on the biofilms of Pseudomonas aeruginosa
The biofilm formation of microorganisms causes persistent tissue infections resistant to treatment with antimicrobial agents. Pseudomonas aeruginosa is commonly isolated from the airways of patients with chronic fibrosis (CF) and often forms biofilms, which are extremely hard to eradicate and a majo...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
She, Pengfei [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015transfer abstract |
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| Schlagwörter: |
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| Umfang: |
7 |
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| Übergeordnetes Werk: |
Enthalten in: Cardio-protective impact of gabapentin against doxorubicin-induced myocardial toxicity in rats; emphasis on modulation of inflammatory-apoptotic signaling - Samra, Yara A. ELSEVIER, 2020, Amsterdam [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:86 ; year:2015 ; pages:38-44 ; extent:7 |
| Links: |
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| DOI / URN: |
10.1016/j.micpath.2015.07.009 |
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ELV023724250 |
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| 245 | 1 | 4 | |a The effects of d-Tyrosine combined with amikacin on the biofilms of Pseudomonas aeruginosa |
| 264 | 1 | |c 2015transfer abstract | |
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| 520 | |a The biofilm formation of microorganisms causes persistent tissue infections resistant to treatment with antimicrobial agents. Pseudomonas aeruginosa is commonly isolated from the airways of patients with chronic fibrosis (CF) and often forms biofilms, which are extremely hard to eradicate and a major cause of mortality and morbidity. Recent studies have shown that d-amino acids (D-AAs) inhibited and disrupted biofilm formation by causing the release of the protein component of the polymeric matrix. However, the effects of D-AAs combined with common antibiotics on biofilms have rarely been studied. The current study first determined whether D-AAs disrupted the biofilms of PAO1 and the clinical airway isolates of P. aeruginosa. It was then determined whether combinations of D-Tyr (the most effective one) and the antibiotic amikacin (AMK) enhanced the activity against these biofilms. The results of the current study showed that D-Tyr is the most effective among those that disassemble the d-amino acids (d-leucine, d-methionine, D-Tyrptophan, and d-tryptophan), and D-Tyr at concentrations higher than 5 mM significantly reduced the biofilm biomass of P. aeruginosa (p < 0.05) without influencing bacterial growth. It was also revealed that D-Tyr improved the efficacy of AMK to combat P. aeruginosa biofilms, as indicated by a reduction in the minimal biofilm-inhibiting concentration (MBIC50 and MBIC90) without a change in the minimal inhibitory concentration (MIC) of planktonic bacteria. Thus, the findings indicated that D-Tyr supplementation overcame the resistance of P. aeruginosa biofilms to AMK, which might be helpful for preventing AMK overuse when this specific D-Tyr is recommended for combatting these biofilms. Also, toxicity of the liver and kidney from AMK could be potentially mitigated by co-delivery with D-Tyr. | ||
| 520 | |a The biofilm formation of microorganisms causes persistent tissue infections resistant to treatment with antimicrobial agents. Pseudomonas aeruginosa is commonly isolated from the airways of patients with chronic fibrosis (CF) and often forms biofilms, which are extremely hard to eradicate and a major cause of mortality and morbidity. Recent studies have shown that d-amino acids (D-AAs) inhibited and disrupted biofilm formation by causing the release of the protein component of the polymeric matrix. However, the effects of D-AAs combined with common antibiotics on biofilms have rarely been studied. The current study first determined whether D-AAs disrupted the biofilms of PAO1 and the clinical airway isolates of P. aeruginosa. It was then determined whether combinations of D-Tyr (the most effective one) and the antibiotic amikacin (AMK) enhanced the activity against these biofilms. The results of the current study showed that D-Tyr is the most effective among those that disassemble the d-amino acids (d-leucine, d-methionine, D-Tyrptophan, and d-tryptophan), and D-Tyr at concentrations higher than 5 mM significantly reduced the biofilm biomass of P. aeruginosa (p < 0.05) without influencing bacterial growth. It was also revealed that D-Tyr improved the efficacy of AMK to combat P. aeruginosa biofilms, as indicated by a reduction in the minimal biofilm-inhibiting concentration (MBIC50 and MBIC90) without a change in the minimal inhibitory concentration (MIC) of planktonic bacteria. Thus, the findings indicated that D-Tyr supplementation overcame the resistance of P. aeruginosa biofilms to AMK, which might be helpful for preventing AMK overuse when this specific D-Tyr is recommended for combatting these biofilms. Also, toxicity of the liver and kidney from AMK could be potentially mitigated by co-delivery with D-Tyr. | ||
| 650 | 7 | |a Amikacin |2 Elsevier | |
| 650 | 7 | |a d-amino acid |2 Elsevier | |
| 650 | 7 | |a Combination |2 Elsevier | |
| 650 | 7 | |a Biofilm |2 Elsevier | |
| 650 | 7 | |a Pseudomonas aeruginosa |2 Elsevier | |
| 650 | 7 | |a d-Tyrosine |2 Elsevier | |
| 700 | 1 | |a Chen, Lihua |4 oth | |
| 700 | 1 | |a Liu, Hongbo |4 oth | |
| 700 | 1 | |a Zou, Yaru |4 oth | |
| 700 | 1 | |a Luo, Zhen |4 oth | |
| 700 | 1 | |a Koronfel, Asmaa |4 oth | |
| 700 | 1 | |a Wu, Yong |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier |a Samra, Yara A. ELSEVIER |t Cardio-protective impact of gabapentin against doxorubicin-induced myocardial toxicity in rats; emphasis on modulation of inflammatory-apoptotic signaling |d 2020 |g Amsterdam [u.a.] |w (DE-627)ELV00536194X |
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10.1016/j.micpath.2015.07.009 doi GBVA2015014000005.pica (DE-627)ELV023724250 (ELSEVIER)S0882-4010(15)00109-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ PHARM DE-84 fid 44.38 bkl She, Pengfei verfasserin aut The effects of d-Tyrosine combined with amikacin on the biofilms of Pseudomonas aeruginosa 2015transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The biofilm formation of microorganisms causes persistent tissue infections resistant to treatment with antimicrobial agents. Pseudomonas aeruginosa is commonly isolated from the airways of patients with chronic fibrosis (CF) and often forms biofilms, which are extremely hard to eradicate and a major cause of mortality and morbidity. Recent studies have shown that d-amino acids (D-AAs) inhibited and disrupted biofilm formation by causing the release of the protein component of the polymeric matrix. However, the effects of D-AAs combined with common antibiotics on biofilms have rarely been studied. The current study first determined whether D-AAs disrupted the biofilms of PAO1 and the clinical airway isolates of P. aeruginosa. It was then determined whether combinations of D-Tyr (the most effective one) and the antibiotic amikacin (AMK) enhanced the activity against these biofilms. The results of the current study showed that D-Tyr is the most effective among those that disassemble the d-amino acids (d-leucine, d-methionine, D-Tyrptophan, and d-tryptophan), and D-Tyr at concentrations higher than 5 mM significantly reduced the biofilm biomass of P. aeruginosa (p < 0.05) without influencing bacterial growth. It was also revealed that D-Tyr improved the efficacy of AMK to combat P. aeruginosa biofilms, as indicated by a reduction in the minimal biofilm-inhibiting concentration (MBIC50 and MBIC90) without a change in the minimal inhibitory concentration (MIC) of planktonic bacteria. Thus, the findings indicated that D-Tyr supplementation overcame the resistance of P. aeruginosa biofilms to AMK, which might be helpful for preventing AMK overuse when this specific D-Tyr is recommended for combatting these biofilms. Also, toxicity of the liver and kidney from AMK could be potentially mitigated by co-delivery with D-Tyr. The biofilm formation of microorganisms causes persistent tissue infections resistant to treatment with antimicrobial agents. Pseudomonas aeruginosa is commonly isolated from the airways of patients with chronic fibrosis (CF) and often forms biofilms, which are extremely hard to eradicate and a major cause of mortality and morbidity. Recent studies have shown that d-amino acids (D-AAs) inhibited and disrupted biofilm formation by causing the release of the protein component of the polymeric matrix. However, the effects of D-AAs combined with common antibiotics on biofilms have rarely been studied. The current study first determined whether D-AAs disrupted the biofilms of PAO1 and the clinical airway isolates of P. aeruginosa. It was then determined whether combinations of D-Tyr (the most effective one) and the antibiotic amikacin (AMK) enhanced the activity against these biofilms. The results of the current study showed that D-Tyr is the most effective among those that disassemble the d-amino acids (d-leucine, d-methionine, D-Tyrptophan, and d-tryptophan), and D-Tyr at concentrations higher than 5 mM significantly reduced the biofilm biomass of P. aeruginosa (p < 0.05) without influencing bacterial growth. It was also revealed that D-Tyr improved the efficacy of AMK to combat P. aeruginosa biofilms, as indicated by a reduction in the minimal biofilm-inhibiting concentration (MBIC50 and MBIC90) without a change in the minimal inhibitory concentration (MIC) of planktonic bacteria. Thus, the findings indicated that D-Tyr supplementation overcame the resistance of P. aeruginosa biofilms to AMK, which might be helpful for preventing AMK overuse when this specific D-Tyr is recommended for combatting these biofilms. Also, toxicity of the liver and kidney from AMK could be potentially mitigated by co-delivery with D-Tyr. Amikacin Elsevier d-amino acid Elsevier Combination Elsevier Biofilm Elsevier Pseudomonas aeruginosa Elsevier d-Tyrosine Elsevier Chen, Lihua oth Liu, Hongbo oth Zou, Yaru oth Luo, Zhen oth Koronfel, Asmaa oth Wu, Yong oth Enthalten in Elsevier Samra, Yara A. ELSEVIER Cardio-protective impact of gabapentin against doxorubicin-induced myocardial toxicity in rats; emphasis on modulation of inflammatory-apoptotic signaling 2020 Amsterdam [u.a.] (DE-627)ELV00536194X volume:86 year:2015 pages:38-44 extent:7 https://doi.org/10.1016/j.micpath.2015.07.009 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-PHARM SSG-OLC-PHA SSG-OPC-PHA 44.38 Pharmakologie VZ AR 86 2015 38-44 7 045F 610 |
| spelling |
10.1016/j.micpath.2015.07.009 doi GBVA2015014000005.pica (DE-627)ELV023724250 (ELSEVIER)S0882-4010(15)00109-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ PHARM DE-84 fid 44.38 bkl She, Pengfei verfasserin aut The effects of d-Tyrosine combined with amikacin on the biofilms of Pseudomonas aeruginosa 2015transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The biofilm formation of microorganisms causes persistent tissue infections resistant to treatment with antimicrobial agents. Pseudomonas aeruginosa is commonly isolated from the airways of patients with chronic fibrosis (CF) and often forms biofilms, which are extremely hard to eradicate and a major cause of mortality and morbidity. Recent studies have shown that d-amino acids (D-AAs) inhibited and disrupted biofilm formation by causing the release of the protein component of the polymeric matrix. However, the effects of D-AAs combined with common antibiotics on biofilms have rarely been studied. The current study first determined whether D-AAs disrupted the biofilms of PAO1 and the clinical airway isolates of P. aeruginosa. It was then determined whether combinations of D-Tyr (the most effective one) and the antibiotic amikacin (AMK) enhanced the activity against these biofilms. The results of the current study showed that D-Tyr is the most effective among those that disassemble the d-amino acids (d-leucine, d-methionine, D-Tyrptophan, and d-tryptophan), and D-Tyr at concentrations higher than 5 mM significantly reduced the biofilm biomass of P. aeruginosa (p < 0.05) without influencing bacterial growth. It was also revealed that D-Tyr improved the efficacy of AMK to combat P. aeruginosa biofilms, as indicated by a reduction in the minimal biofilm-inhibiting concentration (MBIC50 and MBIC90) without a change in the minimal inhibitory concentration (MIC) of planktonic bacteria. Thus, the findings indicated that D-Tyr supplementation overcame the resistance of P. aeruginosa biofilms to AMK, which might be helpful for preventing AMK overuse when this specific D-Tyr is recommended for combatting these biofilms. Also, toxicity of the liver and kidney from AMK could be potentially mitigated by co-delivery with D-Tyr. The biofilm formation of microorganisms causes persistent tissue infections resistant to treatment with antimicrobial agents. Pseudomonas aeruginosa is commonly isolated from the airways of patients with chronic fibrosis (CF) and often forms biofilms, which are extremely hard to eradicate and a major cause of mortality and morbidity. Recent studies have shown that d-amino acids (D-AAs) inhibited and disrupted biofilm formation by causing the release of the protein component of the polymeric matrix. However, the effects of D-AAs combined with common antibiotics on biofilms have rarely been studied. The current study first determined whether D-AAs disrupted the biofilms of PAO1 and the clinical airway isolates of P. aeruginosa. It was then determined whether combinations of D-Tyr (the most effective one) and the antibiotic amikacin (AMK) enhanced the activity against these biofilms. The results of the current study showed that D-Tyr is the most effective among those that disassemble the d-amino acids (d-leucine, d-methionine, D-Tyrptophan, and d-tryptophan), and D-Tyr at concentrations higher than 5 mM significantly reduced the biofilm biomass of P. aeruginosa (p < 0.05) without influencing bacterial growth. It was also revealed that D-Tyr improved the efficacy of AMK to combat P. aeruginosa biofilms, as indicated by a reduction in the minimal biofilm-inhibiting concentration (MBIC50 and MBIC90) without a change in the minimal inhibitory concentration (MIC) of planktonic bacteria. Thus, the findings indicated that D-Tyr supplementation overcame the resistance of P. aeruginosa biofilms to AMK, which might be helpful for preventing AMK overuse when this specific D-Tyr is recommended for combatting these biofilms. Also, toxicity of the liver and kidney from AMK could be potentially mitigated by co-delivery with D-Tyr. Amikacin Elsevier d-amino acid Elsevier Combination Elsevier Biofilm Elsevier Pseudomonas aeruginosa Elsevier d-Tyrosine Elsevier Chen, Lihua oth Liu, Hongbo oth Zou, Yaru oth Luo, Zhen oth Koronfel, Asmaa oth Wu, Yong oth Enthalten in Elsevier Samra, Yara A. ELSEVIER Cardio-protective impact of gabapentin against doxorubicin-induced myocardial toxicity in rats; emphasis on modulation of inflammatory-apoptotic signaling 2020 Amsterdam [u.a.] (DE-627)ELV00536194X volume:86 year:2015 pages:38-44 extent:7 https://doi.org/10.1016/j.micpath.2015.07.009 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-PHARM SSG-OLC-PHA SSG-OPC-PHA 44.38 Pharmakologie VZ AR 86 2015 38-44 7 045F 610 |
| allfields_unstemmed |
10.1016/j.micpath.2015.07.009 doi GBVA2015014000005.pica (DE-627)ELV023724250 (ELSEVIER)S0882-4010(15)00109-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ PHARM DE-84 fid 44.38 bkl She, Pengfei verfasserin aut The effects of d-Tyrosine combined with amikacin on the biofilms of Pseudomonas aeruginosa 2015transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The biofilm formation of microorganisms causes persistent tissue infections resistant to treatment with antimicrobial agents. Pseudomonas aeruginosa is commonly isolated from the airways of patients with chronic fibrosis (CF) and often forms biofilms, which are extremely hard to eradicate and a major cause of mortality and morbidity. Recent studies have shown that d-amino acids (D-AAs) inhibited and disrupted biofilm formation by causing the release of the protein component of the polymeric matrix. However, the effects of D-AAs combined with common antibiotics on biofilms have rarely been studied. The current study first determined whether D-AAs disrupted the biofilms of PAO1 and the clinical airway isolates of P. aeruginosa. It was then determined whether combinations of D-Tyr (the most effective one) and the antibiotic amikacin (AMK) enhanced the activity against these biofilms. The results of the current study showed that D-Tyr is the most effective among those that disassemble the d-amino acids (d-leucine, d-methionine, D-Tyrptophan, and d-tryptophan), and D-Tyr at concentrations higher than 5 mM significantly reduced the biofilm biomass of P. aeruginosa (p < 0.05) without influencing bacterial growth. It was also revealed that D-Tyr improved the efficacy of AMK to combat P. aeruginosa biofilms, as indicated by a reduction in the minimal biofilm-inhibiting concentration (MBIC50 and MBIC90) without a change in the minimal inhibitory concentration (MIC) of planktonic bacteria. Thus, the findings indicated that D-Tyr supplementation overcame the resistance of P. aeruginosa biofilms to AMK, which might be helpful for preventing AMK overuse when this specific D-Tyr is recommended for combatting these biofilms. Also, toxicity of the liver and kidney from AMK could be potentially mitigated by co-delivery with D-Tyr. The biofilm formation of microorganisms causes persistent tissue infections resistant to treatment with antimicrobial agents. Pseudomonas aeruginosa is commonly isolated from the airways of patients with chronic fibrosis (CF) and often forms biofilms, which are extremely hard to eradicate and a major cause of mortality and morbidity. Recent studies have shown that d-amino acids (D-AAs) inhibited and disrupted biofilm formation by causing the release of the protein component of the polymeric matrix. However, the effects of D-AAs combined with common antibiotics on biofilms have rarely been studied. The current study first determined whether D-AAs disrupted the biofilms of PAO1 and the clinical airway isolates of P. aeruginosa. It was then determined whether combinations of D-Tyr (the most effective one) and the antibiotic amikacin (AMK) enhanced the activity against these biofilms. The results of the current study showed that D-Tyr is the most effective among those that disassemble the d-amino acids (d-leucine, d-methionine, D-Tyrptophan, and d-tryptophan), and D-Tyr at concentrations higher than 5 mM significantly reduced the biofilm biomass of P. aeruginosa (p < 0.05) without influencing bacterial growth. It was also revealed that D-Tyr improved the efficacy of AMK to combat P. aeruginosa biofilms, as indicated by a reduction in the minimal biofilm-inhibiting concentration (MBIC50 and MBIC90) without a change in the minimal inhibitory concentration (MIC) of planktonic bacteria. Thus, the findings indicated that D-Tyr supplementation overcame the resistance of P. aeruginosa biofilms to AMK, which might be helpful for preventing AMK overuse when this specific D-Tyr is recommended for combatting these biofilms. Also, toxicity of the liver and kidney from AMK could be potentially mitigated by co-delivery with D-Tyr. Amikacin Elsevier d-amino acid Elsevier Combination Elsevier Biofilm Elsevier Pseudomonas aeruginosa Elsevier d-Tyrosine Elsevier Chen, Lihua oth Liu, Hongbo oth Zou, Yaru oth Luo, Zhen oth Koronfel, Asmaa oth Wu, Yong oth Enthalten in Elsevier Samra, Yara A. ELSEVIER Cardio-protective impact of gabapentin against doxorubicin-induced myocardial toxicity in rats; emphasis on modulation of inflammatory-apoptotic signaling 2020 Amsterdam [u.a.] (DE-627)ELV00536194X volume:86 year:2015 pages:38-44 extent:7 https://doi.org/10.1016/j.micpath.2015.07.009 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-PHARM SSG-OLC-PHA SSG-OPC-PHA 44.38 Pharmakologie VZ AR 86 2015 38-44 7 045F 610 |
| allfieldsGer |
10.1016/j.micpath.2015.07.009 doi GBVA2015014000005.pica (DE-627)ELV023724250 (ELSEVIER)S0882-4010(15)00109-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ PHARM DE-84 fid 44.38 bkl She, Pengfei verfasserin aut The effects of d-Tyrosine combined with amikacin on the biofilms of Pseudomonas aeruginosa 2015transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The biofilm formation of microorganisms causes persistent tissue infections resistant to treatment with antimicrobial agents. Pseudomonas aeruginosa is commonly isolated from the airways of patients with chronic fibrosis (CF) and often forms biofilms, which are extremely hard to eradicate and a major cause of mortality and morbidity. Recent studies have shown that d-amino acids (D-AAs) inhibited and disrupted biofilm formation by causing the release of the protein component of the polymeric matrix. However, the effects of D-AAs combined with common antibiotics on biofilms have rarely been studied. The current study first determined whether D-AAs disrupted the biofilms of PAO1 and the clinical airway isolates of P. aeruginosa. It was then determined whether combinations of D-Tyr (the most effective one) and the antibiotic amikacin (AMK) enhanced the activity against these biofilms. The results of the current study showed that D-Tyr is the most effective among those that disassemble the d-amino acids (d-leucine, d-methionine, D-Tyrptophan, and d-tryptophan), and D-Tyr at concentrations higher than 5 mM significantly reduced the biofilm biomass of P. aeruginosa (p < 0.05) without influencing bacterial growth. It was also revealed that D-Tyr improved the efficacy of AMK to combat P. aeruginosa biofilms, as indicated by a reduction in the minimal biofilm-inhibiting concentration (MBIC50 and MBIC90) without a change in the minimal inhibitory concentration (MIC) of planktonic bacteria. Thus, the findings indicated that D-Tyr supplementation overcame the resistance of P. aeruginosa biofilms to AMK, which might be helpful for preventing AMK overuse when this specific D-Tyr is recommended for combatting these biofilms. Also, toxicity of the liver and kidney from AMK could be potentially mitigated by co-delivery with D-Tyr. The biofilm formation of microorganisms causes persistent tissue infections resistant to treatment with antimicrobial agents. Pseudomonas aeruginosa is commonly isolated from the airways of patients with chronic fibrosis (CF) and often forms biofilms, which are extremely hard to eradicate and a major cause of mortality and morbidity. Recent studies have shown that d-amino acids (D-AAs) inhibited and disrupted biofilm formation by causing the release of the protein component of the polymeric matrix. However, the effects of D-AAs combined with common antibiotics on biofilms have rarely been studied. The current study first determined whether D-AAs disrupted the biofilms of PAO1 and the clinical airway isolates of P. aeruginosa. It was then determined whether combinations of D-Tyr (the most effective one) and the antibiotic amikacin (AMK) enhanced the activity against these biofilms. The results of the current study showed that D-Tyr is the most effective among those that disassemble the d-amino acids (d-leucine, d-methionine, D-Tyrptophan, and d-tryptophan), and D-Tyr at concentrations higher than 5 mM significantly reduced the biofilm biomass of P. aeruginosa (p < 0.05) without influencing bacterial growth. It was also revealed that D-Tyr improved the efficacy of AMK to combat P. aeruginosa biofilms, as indicated by a reduction in the minimal biofilm-inhibiting concentration (MBIC50 and MBIC90) without a change in the minimal inhibitory concentration (MIC) of planktonic bacteria. Thus, the findings indicated that D-Tyr supplementation overcame the resistance of P. aeruginosa biofilms to AMK, which might be helpful for preventing AMK overuse when this specific D-Tyr is recommended for combatting these biofilms. Also, toxicity of the liver and kidney from AMK could be potentially mitigated by co-delivery with D-Tyr. Amikacin Elsevier d-amino acid Elsevier Combination Elsevier Biofilm Elsevier Pseudomonas aeruginosa Elsevier d-Tyrosine Elsevier Chen, Lihua oth Liu, Hongbo oth Zou, Yaru oth Luo, Zhen oth Koronfel, Asmaa oth Wu, Yong oth Enthalten in Elsevier Samra, Yara A. ELSEVIER Cardio-protective impact of gabapentin against doxorubicin-induced myocardial toxicity in rats; emphasis on modulation of inflammatory-apoptotic signaling 2020 Amsterdam [u.a.] (DE-627)ELV00536194X volume:86 year:2015 pages:38-44 extent:7 https://doi.org/10.1016/j.micpath.2015.07.009 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-PHARM SSG-OLC-PHA SSG-OPC-PHA 44.38 Pharmakologie VZ AR 86 2015 38-44 7 045F 610 |
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effects of d-tyrosine combined with amikacin on the biofilms of pseudomonas aeruginosa |
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The effects of d-Tyrosine combined with amikacin on the biofilms of Pseudomonas aeruginosa |
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The biofilm formation of microorganisms causes persistent tissue infections resistant to treatment with antimicrobial agents. Pseudomonas aeruginosa is commonly isolated from the airways of patients with chronic fibrosis (CF) and often forms biofilms, which are extremely hard to eradicate and a major cause of mortality and morbidity. Recent studies have shown that d-amino acids (D-AAs) inhibited and disrupted biofilm formation by causing the release of the protein component of the polymeric matrix. However, the effects of D-AAs combined with common antibiotics on biofilms have rarely been studied. The current study first determined whether D-AAs disrupted the biofilms of PAO1 and the clinical airway isolates of P. aeruginosa. It was then determined whether combinations of D-Tyr (the most effective one) and the antibiotic amikacin (AMK) enhanced the activity against these biofilms. The results of the current study showed that D-Tyr is the most effective among those that disassemble the d-amino acids (d-leucine, d-methionine, D-Tyrptophan, and d-tryptophan), and D-Tyr at concentrations higher than 5 mM significantly reduced the biofilm biomass of P. aeruginosa (p < 0.05) without influencing bacterial growth. It was also revealed that D-Tyr improved the efficacy of AMK to combat P. aeruginosa biofilms, as indicated by a reduction in the minimal biofilm-inhibiting concentration (MBIC50 and MBIC90) without a change in the minimal inhibitory concentration (MIC) of planktonic bacteria. Thus, the findings indicated that D-Tyr supplementation overcame the resistance of P. aeruginosa biofilms to AMK, which might be helpful for preventing AMK overuse when this specific D-Tyr is recommended for combatting these biofilms. Also, toxicity of the liver and kidney from AMK could be potentially mitigated by co-delivery with D-Tyr. |
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The biofilm formation of microorganisms causes persistent tissue infections resistant to treatment with antimicrobial agents. Pseudomonas aeruginosa is commonly isolated from the airways of patients with chronic fibrosis (CF) and often forms biofilms, which are extremely hard to eradicate and a major cause of mortality and morbidity. Recent studies have shown that d-amino acids (D-AAs) inhibited and disrupted biofilm formation by causing the release of the protein component of the polymeric matrix. However, the effects of D-AAs combined with common antibiotics on biofilms have rarely been studied. The current study first determined whether D-AAs disrupted the biofilms of PAO1 and the clinical airway isolates of P. aeruginosa. It was then determined whether combinations of D-Tyr (the most effective one) and the antibiotic amikacin (AMK) enhanced the activity against these biofilms. The results of the current study showed that D-Tyr is the most effective among those that disassemble the d-amino acids (d-leucine, d-methionine, D-Tyrptophan, and d-tryptophan), and D-Tyr at concentrations higher than 5 mM significantly reduced the biofilm biomass of P. aeruginosa (p < 0.05) without influencing bacterial growth. It was also revealed that D-Tyr improved the efficacy of AMK to combat P. aeruginosa biofilms, as indicated by a reduction in the minimal biofilm-inhibiting concentration (MBIC50 and MBIC90) without a change in the minimal inhibitory concentration (MIC) of planktonic bacteria. Thus, the findings indicated that D-Tyr supplementation overcame the resistance of P. aeruginosa biofilms to AMK, which might be helpful for preventing AMK overuse when this specific D-Tyr is recommended for combatting these biofilms. Also, toxicity of the liver and kidney from AMK could be potentially mitigated by co-delivery with D-Tyr. |
| abstract_unstemmed |
The biofilm formation of microorganisms causes persistent tissue infections resistant to treatment with antimicrobial agents. Pseudomonas aeruginosa is commonly isolated from the airways of patients with chronic fibrosis (CF) and often forms biofilms, which are extremely hard to eradicate and a major cause of mortality and morbidity. Recent studies have shown that d-amino acids (D-AAs) inhibited and disrupted biofilm formation by causing the release of the protein component of the polymeric matrix. However, the effects of D-AAs combined with common antibiotics on biofilms have rarely been studied. The current study first determined whether D-AAs disrupted the biofilms of PAO1 and the clinical airway isolates of P. aeruginosa. It was then determined whether combinations of D-Tyr (the most effective one) and the antibiotic amikacin (AMK) enhanced the activity against these biofilms. The results of the current study showed that D-Tyr is the most effective among those that disassemble the d-amino acids (d-leucine, d-methionine, D-Tyrptophan, and d-tryptophan), and D-Tyr at concentrations higher than 5 mM significantly reduced the biofilm biomass of P. aeruginosa (p < 0.05) without influencing bacterial growth. It was also revealed that D-Tyr improved the efficacy of AMK to combat P. aeruginosa biofilms, as indicated by a reduction in the minimal biofilm-inhibiting concentration (MBIC50 and MBIC90) without a change in the minimal inhibitory concentration (MIC) of planktonic bacteria. Thus, the findings indicated that D-Tyr supplementation overcame the resistance of P. aeruginosa biofilms to AMK, which might be helpful for preventing AMK overuse when this specific D-Tyr is recommended for combatting these biofilms. Also, toxicity of the liver and kidney from AMK could be potentially mitigated by co-delivery with D-Tyr. |
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| title_short |
The effects of d-Tyrosine combined with amikacin on the biofilms of Pseudomonas aeruginosa |
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https://doi.org/10.1016/j.micpath.2015.07.009 |
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Chen, Lihua Liu, Hongbo Zou, Yaru Luo, Zhen Koronfel, Asmaa Wu, Yong |
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Chen, Lihua Liu, Hongbo Zou, Yaru Luo, Zhen Koronfel, Asmaa Wu, Yong |
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10.1016/j.micpath.2015.07.009 |
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2024-07-06T19:34:52.341Z |
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