Csg E and Csg F help in the secretion of CsgA and CsgB across the membrane. CsgB is responsible for nucleating CsgA into the fiber across the outer membrane via Csg G secretion complex. CsgA (major subunit) and CsgB (minor subunit) are curli's structural elements which are produced when csg D binds to the promoter of csg BAC operon. It binds to both operons and is responsible for triggering transcription of the csgBACoperon 18. CsgD is the master regulator of curli biogenesis. Curli production is regulated by the two (curli-specific gene) operons csgBAC and csgDEFG 17. These findings suggest that curli biogenesis may be considered as potential targets for developing therapeutics that can attenuate biofilm formation 15.Ĭurli biogenesis is a complicated process that produces curli fibers when enteric bacteria are subjected to stress 16. coli) surface facilitate interbacterial interactions which give bacteria an advantage to invade deeper tissues 13, 14. The curli fimbriae on the UPEC (uropathogenic E. Curli is the primary protein responsible for establishing surface attachment and directing the biofilm's overall structure in enteric biofilms 10, 11, 12. coli biofilms is the curli protein, typically amyloid fibers, which acts in numerous capacities in a biofilm 9, 10. Hence, there is a compelling need to discover antibiotic-sparing anti-biofilm compounds to combat these biofilm-related infections.īiofilms are formed by a wide variety of organisms like Salmonella, Pseudomonas, and Escherichia coli (E.coli) which add to the economic cost of the medical settings 8.The primary structural element of matrix in E. It is thought that the increased microbial resistance is a result of the different cellular metabolism of biofilm cells compared to planktonic cells, as well as the presence of EPS which acts as a diffusion-limiting barrier to antibiotics, thus limiting access to the deeper layers of a biofilm 6, 7. Biofilms-associated infections (e.g., implant-associated infections, urethritis, vaginitis,cystic fibrosis) are generally chronic in which the treatment is quite challenging as cells are embedded in a matrix of extracellular polymeric substances (EPS), making them less susceptible to antimicrobial agents, drugs, and host immunity 3, 4, 5. coli biofilm-related infections.Ī biofilm consists of a complex community of microorganisms that differ from their planktonic counterpart and allow bacteria to survive under extreme conditions such as nutrient depletion and desiccation 1, 2. coli biofilm formation by regulating curli assembly and thus may be used as an alternative therapeutic strategy for the treatment of chronic E. The findings revealed that caffeine could inhibit E. The qRT-PCR data also showed significant downregulation in the expression of CsgBA and the CsgDEFG operon at both 24 mM and 48 mM caffeine. Molecular docking analysis revealed a strong interaction between caffeine and curli regulator protein (Csg D) of E. Caffeine significantly reduced the cytotoxicity and survivability of UPEC. These results were further confirmed by fluorescence microscopy and Scanning Electron Microscope (SEM). coli K-12 by 86.58% and 91.80% respectively at 48 mM caffeine as determined by Crystal Violet assay. coli K-12MG1655.Caffeine significantly reduced the biofilm formation of both UPEC and E. In the present study, we investigated the curli-dependent antibiofilm activity of caffeine against UPEC strain CFT073 and commensal strain E. It is therefore imperative to screen antibiofilm compounds that can impair biofilm formation. coli and other Enterobacteriaceae are curli fibers, making biofilms robust and resistant to antimicrobials. The major component of the extracellular matrix of Uropathogenic E. Biofilms are assemblages of sessile microorganisms that form an extracellular matrix around themselves and mediate attachment to surfaces.
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