Tea polyphenols inhibits biofilm formation, attenuates the quorum sensing-controlled virulence and enhances resistance to Klebsiella pneumoniae infection in Caenorhabditis elegans model.

Bacteria cells can communicate with each other via quorum sensing (QS) system. Various physiological characteristics including virulence factors and biofilm formation are controlled by QS. So interrupting the bacterial communication is an alternative strategy instead of antibiotics for control bacterial infection. The aim of this study was to investigate the effects of tea polyphenols (TPs) on quorum sensing and virulence factors of Klebsiella pneumoniae. In vitro study showed that the anti-QS activity of tea polyphenols against Chromobacterium violaceum in violacein production. At sub-MICs, TPs inhibited the motility, reduced protease and exopolysaccharide (EPS) production and also biofilm formation in K. pneumoniae. In addition, in vivo study showed that tea polyphenols at 200 µg/mL and 400 µg/mL increased the survival rate of Caenorhabditis elegans to 73.3% and 82.2% against K. pneumonia infection. Our findings suggest that tea polyphenols can act as an effective QS inhibitor and can serve as a novel anti-virulence agent for the management of bacterial pathogens.

Shenfu injection for improving cellular immunity and clinical outcome in patients with sepsis or septic shock.

PURPOSE: To assess the efficacy of Shenfu injection (SFI) for enhancing cellular immunity and improving the clinical outcomes of patients with septic shock. METHODS: Patients with sepsis were randomly assigned to receive either SFI at a dose of 100mL every 24hours for 7 consecutive days or a placebo in addition to conventional therapy. The immunologic parameters were collected on days 1, 3, and 7 after the above treatments, and the clinical outcomes were updated for 28days. RESULTS: Of these160 patients, 3 were excluded from the analysis due to protocol violation and withdrawal of consent; thus, 157 completed the study (78 in the SFI group and 79 in the placebo group). We found that SFI increased both CD4+ and CD8+ T cells in peripheral blood and up-regulated HLA-DR expression in monocytes (P<.05). Furthermore, SFI was also found to restore ex vivo monocytic tumor necrosis factor α and interleukin 6 proinflammatory cytokine release in response to the endotoxin (P<.05). Importantly, the SFI group showed better clinical outcomes than did the placebo group in terms of the duration of vasopressor use (P=.008), Acute Physiology and Chronic Health Evaluation II score (P=.034), Marshall score (P=.01), and length of intensive care unit stay (10.5±3.2 vs 12.2±2.8days; P=.012). However, the 28-day mortality rate was not significantly different between the SFI (20.5%; 16/78) and placebo groups (27.8%; -22/79; P=.28). CONCLUSION: These findings suggest that SFI can enhance the cellular immunity of patients with septic shock and could be a promising adjunctive treatment for patients with septic shock.