Antibacterial, antibiofilm, and antivirulence effects of nanoparticles synthesized from Colletotrichum gloeosporioides in pathogenic E. coli

Antimicrobial resistance is a global problem and antibiotics are becoming ineffective due to the resistance developed by bacteria. In this current research, silver nanoparticles were synthesized from aqueous extract of endophytic fungi Colletotrichum gloeosporioides (CgAgNPs) and characterized by various methods. CgAgNPs efficacy was analyzed by performing antimicrobial assays in Escherichia coli ATCC 25922 and antibiotic resistant pathogenic strains. Upon treatment with CgAgNPs biofilm formation was reduced in all E.coli strains. In vitro cytotoxicity assays revealed that CgAgNPs were able to increase the membrane permeability and induced leakage of sugars and proteins. CgAgNPs induced oxidative stress in E. coli strains led to lipid peroxidation and release of malonaldehyde. The CgAgNPs were able to modulate the anti-oxidant system of cells hence there was a reduction in Glutathione reductase, Catalase and Superoxide dismutase enzymes activities. Analysis of expression of gene encoding CTX-M-15 showed the down regulation upon treatment with ampicillin and CgAgNPs. Overall, the results suggest that CgAgNPs control growth, biofilm formation in E. coli through induction of oxidative stress, interference with antioxidant enzymes, cell content leakage and finally downregulating the virulence gene by interfering with transcription and translation in E. coli. In future, CgAgNPs can be incorporated in formulations to break antibiotic resistance in antibiotic resistant pathogenic E. coli.

Automated summary

In this study, silver nanoparticles were synthesized from the aqueous extract of endophytic fungi Colletotrichum gloeosporioides (CgAgNPs) and their antimicrobial activity against Escherichia coli was evaluated. The results showed that CgAgNPs reduced biofilm formation in E. coli by inducing oxidative stress, interfering with antioxidant enzymes, cell content leakage, and downregulating the expression of virulence genes.