Antibacterial activity and mechanism of action of bacteriocin LFX01 against Staphylococcus aureus and Escherichia coli and its application on pork model.

Antibacterial activity and mechanism of action of bacteriocins against bacteria that cause pork contamination remain unclear. Here, antibacterial activity of bacteriocin LFX01 against two important indicator strains (i.e., Staphylococcus aureus and Escherichia coli) and its mechanism of action were investigated. The results showed antibacterial activity of LFX01 against growth and biofilm formation of S. aureus_26 (strain 2612:1606BL1486) and E. coli_02 (strain CMCC(B)44102). Additionally, the results demonstrated that LFX01 could decrease cell metabolic activity, disrupt cell membrane permeability and integrity, and trigger leakage of intracellular contents (e.g., K+, ATP, and lactic dehydrogenase). Furthermore, gel retardation showed that LFX01 could bind to the genomic DNA of indicator strains, disrupting DNA structure. These results uncovered mechanism of action of LFX01 against indicator strains from physiological and phenotypic levels. When applied to the surface of fresh pork models, the antibacterial activity of LFX01 against indicator strains was further confirmed. These findings suggested that LFX01 could be a potential pork preservative for controlling foodborne pathogens.

Antibacterial effect of bacteriocin XJS01 and its application as antibiofilm agents to treat multidrug-resistant Staphylococcus aureus infection.

Multidrug-resistant (MDR) Staphylococcus aureus biofilms have emerged as a serious threat to human health. Recently, the development of antibiotic replacement therapy has gained much attention due to the potential application of bacteriocin. The present study sought to evaluate the antibacterial effect of bacteriocin XJS01 against MDR S. aureus, a previously reported bacteriocin against S. aureus strain 2612:1606BL1486 (S. aureus_26, an MDR strain demonstrated here), and its potential application as an antibiofilm agent. The minimum bactericide concentration of XJS01 against MDR S. aureus_26 was 33.18 µg/mL. XJS01 exhibited excellent storage stability and resistance against acid and reduced the density of established MDR S. aureus_26 biofilm. The hemolytic and HEK293T cytotoxicity activities of XJS01 and the histological analyses in mice confirmed its safety. Moreover, XJS01 effectively disrupted the MDR S. aureus_26 biofilm established on the skin wound surface and reduced the biofilm-isolated bacteria, thereby decreasing the release of pro-inflammatory cytokines and the proliferation of alternatively activated macrophages. Compared to mupirocin, XJS01 exhibited an excellent therapeutic effect on mice skin wounds, confirming it to be a potential alternative to antibiotics.

[Effects of celecoxib combined with radiotherapy on apoptosis of CNE-2Z cell lines].

OBJECTIVE: To investigate the effects of celecoxib combined with radiotherapy on apoptosis of CNE-2Z cell lines and the potential mechanisms. METHODS: Four groups were used, a control, celecoxib (25 micromol/L celecoxib), irradiation (8 Gy X ray) and celecoxib plus irradiation. The radiosensitising effect was detected by clone formation experiment. Flow cytometry was used to detect the apoptosis rate of cells. The expressions of Bcl-2 and Bax were assessed by immunocytochemistry. Western blot was used to examine the expression of Caspase-3. RESULTS: Celecoxib enhanced the radiosensitivity of CNE-2Z cells. In experimental group, the mean surviving fraction and the mean lethal dose of CNE-2Z cells were 0.50 and 2.36 respectively. Compared with the irradiated group, there was significant differences between the two groups (P < 0.01). Celecoxib combined with radiotherapy up-regulation the expression of Bax. The score of the expression of Bax in the control group and the experimental group were 1.221 +/- 0.116 and 2.758 +/- 0.256 respectively. Celecoxib combined with radiotherapy could inhibit the expression of the protein of Bcl-2. The score of the expression of Bcl-2 in the control group and the experimental group were 2.559 +/- 0.144 and 1.253 +/- 0.114 respectively, with significant differences (P < 0.01). Celecoxib combined with radiotherapy could increase the apoptosis rate of tumor cells with significant differences (F = 7.63, P < 0.01). Western blot showed that the expression of Caspase-3 was strengthened. CONCLUSION: Celecoxib combined with radiotherapy could induce apoptosis and enhance the radiosensitivity of human nasopharyngeal carcinoma CNE-2Z cell lines.