Prevention and control of infections have become a formidable challenge due to the increasing resistance of pathogens to antibiotics. Probiotics have been discovered to have positive effects on the host, and it is well-known that some Lactobacilli are effective in treating and preventing inflammatory and infectious diseases. In this study, we developed an antibacterial formulation consisting of honey and Lactobacillus plantarum (honey–L. plantarum). The optimal formulation of honey (10%) and L. plantarum (1 × 10⁹ CFU/mL) was used to investigate its antimicrobial effect and mechanism in vitro, and its healing effect on wound healing of whole skin infections in rats. Biofilm crystalline violet staining and fluorescent staining results indicated that the honey–L. plantarum formulation prevented the biofilm formation in Staphylococcus aureus and Pseudomonas aeruginosa and increased the number of dead bacteria in the biofilms. Further mechanism studies revealed that the honey–L. plantarum formulation may inhibit biofilm formation by upregulating biofilm-related genes (icaA, icaR, sigB, sarA, and agrA) and downregulating quorum sensing (QS) associated genes (lasI, lasR, rhlI, rhlR, and pqsR). Furthermore, the honey–L. plantarum formulation decreased the number of bacteria in the infected wounds of rats and accelerated the formation of new connective tissue to promote wound healing. Our study suggests that the honey–L. plantarum formulation provides a promising option for the treatment of pathogenic infections and wound healing.

Pseudomonas aeruginosa is known to generate bacterial biofilms that increase antibiotic resistance. With the increase of multi-drug resistance in recent years, the formulation of a new therapeutic strategy has seemed urgent. Preliminary findings show that Prodigiosin (PG), derived from chromium-resistant Serratia marcescens, exhibited efficient anti-biofilm activity against Staphylococcus aureus. However, its anti-biofilm activity against P. aeruginosa remains largely unexplored. The anti-biofilm activity of PG against three clinical single drug-resistant P. aeruginosa was evaluated using crystal violet staining, and the viability of biofilms and planktonic cells were also assessed. A model of chronic lung infection was constructed to test the in vivo antibiofilm activity of PG. The results showed that PG inhibited biofilm formation and effectively inhibited the production of pyocyanin and extracellular polysaccharides in vitro, as well as moderated the expression of interleukins (IL-1β, IL-6, IL-10) and tumor necrosis factor (TNF-α) in vivo, which might be attributed to the downregulation of biofilm-related genes such as algA, pelA, and pslM. These findings suggest that PG could be a potential treatment for drug-resistant P aeruginosa and chronic biofilm infections.

Objective: Serratia sp. CM01 is a naturally domesticated strain with chromium (Cr) resistance and Cr(VI) reduction ability isolated from a Cr-enriched environment. The genome of Serratia sp. CM01 was sequenced and analysed to identify key genes involved in chromium metabolism. Corresponding engineered bacteria associated with special metabolic features were constructed to further study the function of these genes and their encoded proteins in chromium metabolism. Methods: The whole genome of Serratia sp. CM01 was sequenced, and genes involved in chromium metabolism were analysed. The ChrA1 and Srpc genes were selected and introduced into E. coli using the prokaryotic expression vector pET-28a. The target proteins were identified using sodium dodecyl sulphate‒polyacrylamide gel electrophoresis (SDS‒PAGE) and Western blotting. Chromium tolerance and removal tests were used to assess the chromium metabolic capabilities of the engineered bacteria. Results: The results of genome sequencing revealed that the genome size of Serratia sp. was 4,902,254 bp, from which 12 genes involved in chromium metabolism were screened. The ChrA1 and Srpc genes were chosen, and three engineered bacteria (eChrA1, eSrpc, and eCS) were successfully constructed. The growth of the three engineered bacteria showed no difference under Cr(VI)-free circumstances (P > 0.05). In the presence of Cr(VI), the viable bacterial cell mount during the stabilization phase was eCS > eChrA1 > eSrpc, and the tolerance and removal rate of Cr(VI) was ranked eCS > eChrA1 > eSrpc. Conclusion: The genome of Serratia sp. CM01 contains genes related to chromium metabolism, such as NemA, ChrA1, Srpc and FieF. The ChrA1 and Srpc gene-encoded proteins confer Cr(VI) resistance to engineered bacteria, but the specific mechanism of chromium resistance remains to be further studied. eChrA1 has a stronger anti-Cr(VI) ability than eSrpc. The eCS-engineered bacterial strain with ChrA1 and Srpcgenes was more resistant to hexavalent chromium, and it has the potential to handle Cr(VI) pollution in the virtual environment.