Probiotics are known to provide the host with immune-modulatory effects and are therefore of remarkable interest for therapeutic and prophylactic applications against various disorders, including inflammatory diseases. Weissella cibaria JW15 (JW15) has been reported to possess probiotic and antioxidant properties. However, the effect of JW15 on inflammatory responses has not yet been reported. Therefore, the objective of the current study was to evaluate the anti-inflammatory potential of JW15 against lipopolysaccharide (LPS) stimulation. The production of pro-inflammatory factors and the cellular signaling pathways following treatment with heat-killed JW15 was examined in LPS-induced RAW 264.7 cells. Treatment with heat-killed JW15 decreased nitric oxide and prostaglandin E 2 production via downregulation of the inducible nitric oxide synthase and cyclooxygenase-2. In addition, treatment with heat-killed JW15 suppressed the expression of pro-inflammatory cytokines, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α. The anti-inflammatory properties of treating with heat-killed JW15 were associated with mitogen-activated protein kinase signaling pathwaymediated suppression of nuclear factor-κB. These results indicated that JW15 possesses antiinflammatory potential and provide a molecular basis regarding the development of functional probiotic products.

The objective of this study was to evaluate the functional properties of Weissella cibaria JW15 (JW15) by investigating its antagonistic and antioxidant activities. Lactobacillus rhamnosus GG (LGG) was used for comparison as a reference strain. JW15 inhibited the growth of pathogenic bacteria (Listeria monocytogenes, Salmonella Typhimurium, S. Enteritidis, and Escherichia coli). Compared to LGG, JW15 showed rapid organic acid production, with the amounts of lactic and acetic acids being lower and higher, respectively. In addition, JW15 significantly inhibited intestinal epithelial adherence in the tested pathogens. JW15 exhibited antioxidant effects by scavenging radicals including DPPH, ABTS, and hydroxyl radicals, and inhibiting lipid peroxidation. JW15 exhibited significant antagonistic and antioxidant activities compared to LGG in the tested assay (p \ 0.05). The results suggested that JW15 might possess a potential for amelioration of disorders induced by pathogenic bacteria or oxidative stress.

Transforming growth factor (TGF)‐β1 directs class switch recombination (CSR) to IgG2b as well as to IgA. Smad3/4, Runx3 and p300 mediate TGF‐β1‐induced germ‐line (GL) α transcription leading to IgA expression. However, the molecular mechanisms by which TGF‐β1 induces IgG2b CSR are unknown. We used luciferase reporter plasmids to investigate how TGF‐β1 regulates the activity of the promoter for GL transcripts of IgG2b constant gene (GLγ2b promoter). Similarly to the GLα promoter, overexpression of Smad3/4 and Runx3 enhances TGF‐β1‐induced GLγ2b promoter activity. Mutation analysis of the promoter identified likely Smad‐ and Runx3‐binding sites. Also similar to the GLα promoter, overexpression of p300 enhances Smad3/4‐mediated promoter activity, whereas E1A represses promoter activity. Since these regulation mechanisms underlying both GLα and GLγ2b transcription are similar, we explored the possibility that TGF‐β1 induces IgA CSR via transitional IgG2b CSR. TGF‐β1 enhances the expression of both Iα‐Cμ and Iα‐Cγ2b circle transcripts, indicative of direct (Sμ→Sα) and sequential CSR (Sμ→Sγ2b→Sα).

The status of the GP130-STAT3 signaling pathway in humans with nonalcoholic fatty liver disease (NAFLD) and its relevance to disease pathogenesis are unknown. The expression of the gp130-STAT3 axis and gp130 cytokine receptors were studied in subjects with varying phenotypes of NAFLD including nonalcoholic steatohepatitis (NASH) and compared with lean and weight-matched controls without NAFLD. Gp130 and its downstream signaling element (Tyk2 and STAT3) expression were inhibited in obese controls whereas they were increased in NAFLD. IL-6 levels were increased in NASH and correlated with gp130 expression (P < 0.01). Palmitate inhibited gp130-STAT3 expression and signaling. IL-6 and palmitate inhibited hepatic insulin signaling via STAT3-dependent and independent mechanisms, respectively. STAT3 overexpression reversed palmitate-induced lipotoxicity by increasing autophagy (ATG7) and decreasing endoplasmic reticulum stress. These data demonstrate that the STAT3 pathway is activated in NAFLD and can worsen insulin resistance while protecting against other lipotoxic mechanisms of disease pathogenesis.

Dietary supplementation with lactic acid bacteria to maintain or improve intestinal health is advocated. Weissella spp. are present in different fermented vegetable‐based foods like kimchi, as well as in the normal gastrointestinal (GI) tract of humans. Weissella cibaria strains have been proposed as potential probiotics. Freeze‐drying is a promising treatment method for these strains for industrial applications and to increase the accessibility of their health‐promoting benefits. Moreover, probiotic strains need to be able to survive in the host GI tract, and acid and bile are both environmental stressors that can reduce strain survival. Therefore, this study evaluated the effect of the combination of protective agents on the acid and bile resistance of W. cibaria JW15 after freeze‐drying. A protective agent combination with a 1:1 ratio of 5 g + 5 g/100 ml w/v soy flour + yeast extract (SFY) retained nearly 100% viability after freeze‐drying and was resistant to artificial bile acids. Remarkably, skim milk + soy flour (SSF) was resistant to an acidic solution, and the viability of W. cibaria JW15 in artificial gastric acid was enhanced when treated with this mixture. Furthermore, SFY and SSF were found to maintain high numbers of viable cells with a low specific rate of cell death (k) after storage at 50°C, 60°C, and 70°C. These results support an effective probiotic formulation system with a high number of viable cells, and its protective effects can be leveraged in the development of probiotic products with health benefits.

The balloon flower (BF) is a potent natural source of phytochemical compounds and is associated with our health. The sprouting process is accompanied by significant changes in phytochemical compounds in comparison with their original plants. Even though many studies are conducted with BF, there are not yet reports of BF sprouts.In the present study, we determined the chemical composition and biological activity of BF sprouts that had been cultivated for 50 days. Kaempferol-3-O-galactoside and 1-O-caffeoylquinic acid were identified as major components of whole BF sprouts.The leaves/stems of the sprouts had higher total phenolic and flavonoid contents and lower IC 50 values in DPPH • and ABTS •+ scavenging assays than whole sprouts or roots. The roots of the sprouts had the highest polygalacin D content (1.44 mg/g).We also determined the effects of different parts of BF sprouts on RAW 264.7 macrophage cells. When these cells were stimulated with lipopolysaccharide (LPS), their nitrite and pro-inflammatory cytokine production increased. BF sprouts suppressed the LPS-induced production of nitrite, tumor necrosis factor-α, and interleukin-6 in a concentration-dependent manner without causing any cytotoxic effects. Nitrite and pro-inflammatory cytokine production were significantly inhibited by the roots and leaves/stems, respectively. The inhibitory effects of BF sprouts on LPS-stimulated inflammatory responses in RAW 264.7 macrophage cells were associated with suppressed NF-κB activation. These findings suggest that BF sprouts could be a valuable source of bioactive compounds and exert anti-inflammatory effects due to their polygalacin D, deapi-platycodin D 3, and polyphenol content. K E Y W O R D Sflavonoid, platycodi radix, polyphenol, root, saponin, sprout | 247 KIM et al.

Objectives High mobility group box 1 (HMGB1) is a chromatin-binding protein located in the cell nucleus. Following injury, immunocompetent cells secrete HMGB1 to the extracellular milieu under the stimulation of pro-inflammatory cytokines. Extracellular HMGB1 acts a “danger signal” that instigates the innate immunity and tissue repair. We previously reported HMGB1 in the vocal fold extracellular compartment between Day 3 and Day 7 following surgical injury. In this study, we further investigated the cell source of HMGB1 and the relationship of pro-inflammatory cytokine expression and HMGB1 translocation in wounded vocal folds. Study Design Prospective animal study. Methods Bilateral vocal fold injury was performed on 122 Sprague-Dawley rats. An additional 18 rats served as uninjured controls. Animals were sacrificed at multiple time points up to 4 weeks after surgery. Immunohistochemistry co-staining was performed to identify the cell source of HMGB1. Cell markers, ED1, fibroblast-specific protein 1 (FSP1), and alpha smooth muscle actin (α-SMA) were used to identify macrophages, fibroblasts and myofibroblasts respectively. Enzyme-linked immunosorbent assays were performed to measure cytokine levels of interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) in vocal fold tissue. Results Co-staining of HMGB1 was strong with ED1 and FSP1 but was minimal with α-SMA in injured vocal folds. Compared to uninjured controls, IL-1β and TNF-α expression increased significantly the first two days after injury. Conclusions Macrophages and fibroblasts were a major cell source of vocal fold HMGB1. Translocation of HMGB1 may be an active response to the early accumulation of IL-1β and TNF-α in the wounded vocal folds.

We designed and assembled a simulated human intestinal system (SHIS) consisting of a stomach and a small intestine. Each reactor vessel has several ports such as the input and output of medium, a sampler of liquid phase, a pH electrode, a pH control (acid and base), and a thermometer. The SHIS was kept at body temperature (37°C) by pumping water into the space between the jacket and the inside walls. The stomach chamber was initially filled with gas fluids and then digested for 2 hr. After the stomach digestion, the residuals was delivered from stomach chamber into the small intestine chamber by secreting intestinal fluid for 4 hr, followed by secretion of 0.3M NaHCO 3 , 0.1M NaHCO 3 , 4% bile salt, and 2% bile salt for 1, 3, 0.5, and 3.5 hrs, respectively. In order to prepare the alginate/chitosan capsule as a delivery system for bioactive agents, the microencapsulation system was assembled with a control unit, a electrical, a pneumatic systems, and a reaction vessel. After digestion of alginate capsules, the content of total sugar was 7.47% and 60.82% in the stomach and small intestine (simulated human intestinal system, SHIS), respectively. However, in case of alginate/chitosan capsule and alginate/chitosan capsule coated with polyacryl emulsion (alginate/chitosan-PAE), the total sugar content were 3.12 and 4.62% in the stomach model and 43.46 and 42.09% in the small intestine model, respectively. There were no difference on the degree of digestion in the alginate capsule and alginate/polyethylene glycol (alginate/PEG) capsule prepared with 0.1-0.3% of PEG in the stomach model. As a result, the alginate matrix remained in a shrunken state due to conversion of sodium alginate into insoluble alginic acid, which acted as a barrier to chitosan microparticles. And it was effective for digesting by intestinal fluid and releasing of the sugar.