Background: The endothelial glycocalyx layer (EGL) coats the alveolar capillary endothelium and plays important roles in pulmonary vascular protection, modulation, and hemostasis. Ischemia-reperfusion, which occurs during lung resection surgery with one lung ventilation (OLV), can damage the EGL. Sevoflurane is known for its protective effect against ischemia-reperfusion injury. Therefore, we hypothesized that lung resection surgery produces EGL damage and sevoflurane protects the EGL better than the intravenous anesthetic propofol. Methods: Seventy-eight patients undergoing pulmonary resection were randomly allocated into the sevoflurane (n=38) and propofol (n=40) groups. All patients received OLV and protective ventilation under sevoflurane-or propofol-based anesthesia. The concentrations of EGL injury markers (heparan sulfate and human syndecan-1) and an inflammatory marker (vascular cell adhesion molecule-1) were measured from blood samples drawn at five time points (after induction, 60 min after OLV, 120 min after OLV, end of OLV, and end of surgery). Results: OLV increased the concentrations of EGL injury markers; heparan sulfate concentrations increased from 120 minutes after OLV (120 minutes after OLV: sevoflurane, 13.3±6.8 ng/mL, P<0.05; propofol, 14.8±6.9 ng/mL, P<0.05). Human syndecan-1 concentrations also increased from 120 minutes after OLV (120 minutes after OLV: sevoflurane, 20.4±8.9 ng/mL, P<0.05; propofol, 20.5±11.8 ng/mL, P>0.05). However, no difference in EGL injury markers was observed between the sevoflurane and propofol groups at any time point. Vascular cell adhesion molecule-1 concentrations did not show any temporal changes in either group. Conclusions: Lung resection surgery with OLV produced EGL damage without any increase in inflammation. Although shedding of heparan sulfate induced by EGL injury during lung resection surgery with OLV, was less than propofol, it was not statistically significant.

Vitamin B2, also known as riboflavin, is essential for maintaining human health. The purpose of this study was to isolate novel lactic acid bacteria that overproduce vitamin B2 and to validate their potential as probiotics. In this study, Lactobacillus plantarum HY7715 (HY7715) was selected among lactic acid bacteria isolated from Kimchi. HY7715 showed a very high riboflavin-producing ability compared to the control strain due to the high expression of ribA, ribB, ribC, ribH, and ribG genes. HY7715 produced 34.5 ± 2.41 mg/L of riboflavin for 24 h without consuming riboflavin in the medium under optimal growth conditions. It was able to produce riboflavin in an in vitro model of the intestinal environment. In addition, when riboflavin deficiency was induced in mice through nutritional restriction, higher levels of riboflavin were detected in plasma and urine in the HY7715 administration group than in the control group. HY7715 showed high survival rate in simulated gastrointestinal conditions and had antibiotic resistance below the cutoff MIC value suggested by the European Food Safety Authority; moreover, it did not cause hemolysis. In conclusion, HY7715 could be considered a beneficial probiotic strain for human and animal applications, suggesting that it could be a new alternative to address riboflavin deficiency.

Lactobacillus acidophilus species are well-known probiotics with the beneficial activity of regulating cholesterol levels. In this study, we showed that L. acidophilus K301 reduced the level of cholesterol through reverse transport in macrophages. L. acidophilus K301 upregulated the mRNA and protein levels of genes such as ATP-binding cassette A1 (ABCA1) and ATP-binding cassette G1 (ABCG1) under the control of liver X receptor (LXR), resulting in increased apoA-I-dependent cholesterol efflux in phorbol 12-myristate 13-acetate (PMA)-differentiated THP-1 cells. L. acidophilus K301 induced both ABCA1 and ABCG1 through the endogenous LXR agonist 24(S), 25-epoxcycholesterol, which is synthesized by intracellular cholesterol synthetic pathways. In vivo studies using L. acidophilus K301-treated ApoE-/- mice showed reduced accumulation of lipoproteins in the arterial lumen. The inhibitory effects of L. acidophilus K301 on accumulation of lipoprotein in atherosclerotic plaques were mediated by the induction of squalene reductase (SQLE) and oxidosqualene cyclase (OSC) and resulted in ABCA1-mediated cholesterol efflux. Taken together, our findings revealed that Lactobacillus acidophilus K301 regulates the expression of genes related to cholesterol reverse transport via the induction of endogenous LXR agonist, suggesting the therapeutic potential of Lactobacillus acidophilus K301 as an anti-atherosclerotic agent.

Epidemiological studies have shown that exposure to particulate matter (PM) is associated with adverse health effects. Inhalation of fine particulate matter (PM2.5) is associated with elevated pulmonary diseases. However, the molecular mechanism underlying the initiation of lung inflammation following inhalation is unclear. In this study, we investigated the beneficial effects of two probiotics, Lactobacillus casei HY2782 and Bifidobacterium lactis HY8002, against PM-induced pulmonary inflammation. Model mice were subjected to chronic exposure of PM2.5. The results showed that PM2.5 enhanced oxidative stress and led to Th2 cytokine responses in the mice. PM2.5-exposed mice were orally administered with HY2782 and HY8002 from the day of first exposure to the end point of the study. The results showed that HY2782 ameliorated PM 2.5 exposure-enhanced leukocyte migration and activation of proinflammatory cytokines. HY2782 and HY8002 also prevented exacerbation of eosinophil and neutrophil infiltration in the bronchoalveolar lavage fluid. HY2782 and HY8002 significantly increased scavenging of PM2.5-induced reactive oxygen species and activated superoxide dismutase and catalase activity in the blood. These results indicate that the probiotics HY2782 and HY8002 protect against PM-induced pulmonary inflammation.

The effect of standard therapeutic strategies on Helicobacter pylori infection is diminished over time owing to the emergence of drug resistant strains. In this study, we would like to confirm the enhanced effect of L. paracasei HP7, which has been reported to exert antibacterial and gastric mucosal protective effects, in combination with Perilla frutescens var. acuta (P. frutescens)and Glycyrrhiza glabra (G. glabra) extracts. P. frutescens extract and G. glabra extract were found to inhibit the growth of H. pylori in a concentration-dependent manner, and the combination of L. paracasei HP7 and P. frutescens extract and G. glabra extract effectively inhibited H. pylori from attaching to AGS a gastric epithelial cells. Moreover, L. paracasei HP7 complex mixture containing P. frutescens and G. glabra extracts has been shown to inhibit H. pylori virulence genes such as AlpA, CagA, FlaA and UreA. When H. pylori-infected mice were administered a complex mixture of L. paracasei HP7 containing P. frutescens and G. glabra extract, the infection rate of H. pylori was significantly reduced. In addition, the L. paracasei HP7 complex mixture significantly reduced serum IL-8 levels and stomach inflammation in H. pylori infected mice. These results suggest that a complex mixture of L. paracasei HP7 containing P. frutescens and G. glabra extracts may be an alternative to treating diseases caused by H. pylori infection.

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