Search

Engineering living functional biofilms offers an ecofriendly and efficient technique for the corrosion protection of metallic materials in marine environments. Its firm attachment to the metal surface is a key step to effectively improve the corrosion protection. Herein, engineered Escherichia coli biofilm with strong metal binding ability is constructed by genetically appending a metal binding domain (MBD) to extracellular amyloids. The engineered living biofilm improved the corrosion resistance of X70 carbon steel. Moreover, a biofilm‐induced mineralization layer, mainly composed of calcite, is formed on the X70 surface, which provided a stable corrosion barrier. At the end of 7‐days immersion, the icorr decreased from 5.1 ± 0.4 µA cm−2 without biofilm to 0.5 ± 0.1 µA cm−2 with E. coli MBD biofilm, resulting in a corrosion inhibition efficiency of 90.2%. It also demonstrated the corrosion protection effect for 304 stainless steel, suggesting possible broad applications of the engineered biofilm. The application of synthetic biology offers a novel approach in the development of anti‐corrosion technologies in water environments. [ABSTRACT FROM AUTHOR]

Clostridioides difficile infection (CDI) with high morbidity and high mortality is an urgent threat to public health, and C. difficile pathogenesis studies are eagerly required for CDI therapy. The major surface layer protein, SlpA, was supposed to play a key role in C. difficile pathogenesis; however, a lack of isogenic slpA mutants has greatly hampered analysis of SlpA functions. In this study, the whole slpA gene was successfully deleted for the first time via CRISPR-Cas9 system. Deletion of slpA in C. difficile resulted in smaller, smother-edged colonies, shorter bacterial cell size, and aggregation in suspension. For life cycle, the mutant demonstrated lower growth (changes of optical density at 600 nm, OD600) but higher cell density (colony-forming unit, CFU), decreased toxins production, and inhibited sporulation. Moreover, the mutant was more impaired in motility, more sensitive to vancomycin and Triton X-100-induced autolysis, releasing more lactate dehydrogenase. In addition, SlpA deficiency led to robust biofilm formation but weak adhesion to human host cells.IMPORTANCE Clostridioides difficile infection (CDI) has been the most common hospital-acquired infection, with a high rate of antibiotic resistance and recurrence incidences, become a debilitating public health threat. It is urgently needed to study C. difficile pathogenesis for developing efficient strategies as CDI therapy. SlpA was indicated to play a key role in C. difficile pathogenesis. However, analysis of SlpA functions was hampered due to lack of isogenic slpA mutants. Surprisingly, the first slpA deletion C. difficile strain was generated in this study via CRISPR-Cas9, further negating the previous thought about slpA being essential. Results in this study will provide direct proof for roles of SlpA in C. difficile pathogenesis, which will facilitate future investigations for new targets as vaccines, new therapeutic agents, and intervention strategies in combating CDI., Competing Interests: The authors declare no conflict of interest.