Lentibacillus kimchii sp. nov., an extremely halophilic bacterium isolated from kimchi, a Korean fermented vegetable.

A Gram-positive, aerobic, non-motile and extremely halophilic bacterial strain, designated K9(T), was isolated from kimchi, a Korean fermented food. The strain was observed as endospore-forming rod-shaped cells showing oxidase and catalase activity. It was found to grow at 10.0-30.0 % (w/v) NaCl (optimum, 15.0-20.0 %), pH 7.0-8.0 (optimum, pH 7.5) and 15-40 °C (optimum, 30 °C). The polar lipids of strain K9(T) were identified as phosphatidylglycerol, three unidentified phospholipids and an unidentified glycolipid. The isoprenoid quinone was identified as menaquinone-7. The major cellular fatty acids (>20 % of the total) were found to be anteisio-C15:0 and anteisio-C17:0. The cell wall peptidoglycan composition was determined to contain meso-diaminopimelic acid. The G + C content of genomic DNA was determined to be 48.2 mol %. Phylogenetic analysis based on the 16S rRNA gene sequence revealed that the isolated strain is closely related to Lentibacillus salinarum AHS-1(T) (96.7 % sequence similarity). Based on its phenotypic, chemotaxonomic and phylogenetic data, strain K9(T) is considered to represent a novel species of the genus Lentibacillus, for which the name Lentibacillus kimchii sp. nov., is proposed. The type strain is K9(T) (=KACC 18490(T) = JCM 30234(T)).

High glucose-induced O-GlcNAcylated carbohydrate response element-binding protein (ChREBP) mediates mesangial cell lipogenesis and fibrosis: the possible role in the development of diabetic nephropathy.

Carbohydrate response element-binding protein (ChREBP) is a transcription factor responsible for carbohydrate metabolism in the liver. However, the role of ChREBP in diabetic nephropathy has not been elucidated. Thus, we investigated the role of ChREBP in mesangial cells in diabetic nephropathy. Treatment with 25 mM glucose (high glucose; HG) increased cellular O-GlcNAc and O-GlcNAcylated ChREBP in mesangial cells compared with normal 5.5 mM glucose. O-(2-acetamido-2-deoxy-D-glucopyranosylidene) amino N-phenylcarbamate (PUGNAc), a drug that increases O-GlcNAc, augmented the expression of ChREBP targets, whereas DON, a drug that decreases O-GlcNAc and O-GlcNAcase overexpression, mitigated the increase with HG. O-GlcNAc augmented the protein stability, transcriptional activity, and nuclear translocation of ChREBP. HG treatment also stimulated lipid accumulation and the contents of triglyceride and cholesterol in mesangial cells. In addition, HG triggered expression of hypoxia-inducible factor 1-α, vascular endothelial growth factor, and extracellular matrix components related to nephrosclerosis. The ChREBP mutant, W130A, did not exhibit HG-induced lipid accumulation and fibrotic proteins, suggesting that the Trp-130 residue in the MCR3 domain is important in the development of glomerulosclerosis. O-GlcNAcylated ChREBP was elevated in mesangium cells of streptozotocin-induced diabetic rats. In conclusion, HG increased the O-GlcNAcylated ChREBP level, which resulted in lipid accumulation and up-regulation of fibrotic proteins in mesangial cells. These effects may lead mesangial cells to an ultimately pathological state.

Inhibitory effect of cucurbitacin B on imiquimod-induced skin inflammation.

Psoriasis is a common skin disease, of which pathogenesis involves the increase of inflammatory reaction in epidermal cells. In an attempt to find therapeutics for psoriasis, we found that cucurbitacin B has an inhibitory potential on imiquimod-induced inflammation of keratinocytes. Cucurbitacin B significantly inhibited imiquimod-induced expression of crucial psoriatic cytokines, such as IL-8 and CCL20, via down-regulation of NF-κB and STAT3 signaling pathway in human keratinocytes. In addition, keratinocyte proliferation was markedly inhibited by cucurbitacin B. The potential beneficial effect of cucurbitacin B on psoriasis was further validated in imiquimod-induced psoriasiform dermatitis of experimental animal. Topical application of cucurbitacin B resulted in significant reduction of epidermal hyperplasia and inflammatory cytokines production, and ameliorated the psoriatic symptom. Taken together, these results suggest that cucurbitacin B may be a potential candidate for the treatment of psoriasis.

Identification of a possible susceptibility locus for UVB-induced skin tanning phenotype in Korean females using genomewide association study.

A two-stage genomewide association (GWA) analysis was conducted to investigate the genetic factors influencing ultraviolet (UV)-induced skin pigmentation in Korean females after UV exposure. Previously, a GWA study evaluating ~500 000 single nucleotide polymorphisms (SNPs) in 99 Korean females identified eight SNPs that were highly associated with tanning ability. To confirm these associations, we genotyped the SNPs in an independent replication study (112 Korean females). We found that a novel SNP in the intron of the WW domain-containing oxidoreductase (WWOX) gene yielded significant replicated associations with skin tanning ability (P-value = 1.16 × 10(-4) ). To understand the functional consequences of this locus located in the non-coding region, we investigated the role of WWOX in human melanocytes using a recombinant adenovirus expressing a microRNA specific for WWOX. Inhibition of WWOX expression significantly increased the expression and activity of tyrosinase in human melanocytes. Taken together, our results suggest that genetic variants in the intronic region of WWOX could be determinants in the UV-induced tanning ability of Korean females. WWOX represents a new candidate gene to evaluate the molecular basis of the UV-induced tanning ability in individuals.

Thioredoxin-interacting protein mediates hepatic lipogenesis and inflammation via PRMT1 and PGC-1α regulation in vitro and in vivo.

BACKGROUND & AIMS: Non-alcoholic fatty liver disease (NAFLD) is strongly associated with obesity and type 2 diabetes. Thioredoxin-interacting protein (TXNIP) regulates the cellular redox state and metabolism and has been linked to many diseases, including diabetes. Therefore, we examined the role of TXNIP in hepatic steatosis in vitro and in vivo. METHODS: Lipogenic and inflammatory proteins produced by hepatocytes treated with palmitic acid (PA) or transfected with TXNIP or Txnip siRNA were measured by Western blotting. Lipid accumulation was assessed using Oil Red O staining. Protein interactions were assessed by immunoprecipitation and proximity ligation assay. Hepatic protein levels were measured by Western blotting from wild type or Txnip(-/-) mice fed a high-fat diet (HFD) or chow diet. Livers from NAFLD patients were compared with normal liver by immunohistochemistry. RESULTS: PA increased TXNIP, and inflammatory and lipogenic proteins in both AML12 and H4IIE cells. It also increased the peroxisome proliferator-activated receptor gamma co-activator-1α (PGC-1α), which mediated the expression of lipogenic markers and lipid accumulation. In addition, PA increased protein arginine methyltransferase-1 (PRMT1) and PRMT1 siRNA abolished the increase in lipogenic markers with PGC-1α. Furthermore, TXNIP interacted with PRMT1 in PA-treated hepatocytes. In vivo, levels of lipogenic proteins, inflammatory molecules, PGC-1α, and PRMT1 were increased in the livers of HFD mice compared with those fed a chow diet, and were ameliorated in HFD Txnip(-/-) mice. Moreover, TXNIP, PRMT1, and PGC-1α were elevated in the livers of human NAFLD patients. CONCLUSIONS: TXNIP mediates hepatic lipogenesis via PRMT1 and PGC-1α regulation and inflammation in vitro and in vivo, implying that targeting TXNIP and PRMT1 is a potential therapeutic approach for treatment of NAFLD.

High-glucose-induced CARM1 expression regulates apoptosis of human retinal pigment epithelial cells via histone 3 arginine 17 dimethylation: role in diabetic retinopathy.

Hyperglycemia-induced apoptosis of retinal pigment epithelial (RPE) cells is considered to be involved in the progression of diabetic retinopathy. Histone arginine methylation catalyzed by protein arginine methyltransferases (PRMTs) has emerged as an important histone modification involved in gene regulation. However, the role of PRMTs in diabetic retinopathy has not been elucidated. Here, we found that expression of coactivator-associated arginine methyltransferase 1 (CARM1; also known as PRMT4) was increased in the high-glucose treated human RPE cell line ARPE-19 and in the RPE layer of streptozotocin-treated rats. In addition, high-glucose induced apoptosis in ARPE-19 cells. To determine the function of CARM1 on RPE cell apoptosis, we performed gain- and loss-of-function studies. CARM1 overexpression increased apoptosis of RPE cells. In contrast, silencing of CARM1 expression by siRNA and pharmacological inhibition of CARM1 activity abolished high-glucose-induced RPE cell apoptosis. Furthermore, we found that inhibition of histone 3 arginine 17 (H3R17) asymmetric dimethylation attenuates both CARM1- and high-glucose-induced apoptosis in RPE cells. Together, these results show that high-glucose-induced CARM1 expression increases RPE cell apoptosis via H3R17 asymmetric dimethylation. Strategies to reduce CARM1 expression or enzymatic activity could be used to prevent apoptosis of RPE cells in the progression of diabetic retinopathy.

Activation of PRMT1 and PRMT5 mediates hypoxia- and ischemia-induced apoptosis in human lung epithelial cells and the lung of miniature pigs: the role of p38 and JNK mitogen-activated protein kinases.

Severe hypoxic and ischemic injury leads to primary graft dysfunction after lung transplantation. Arginine methylation, which is responsible for the regulation of a variety of biological functions, is mediated by protein arginine methylation transferases (PRMTs). This study examined the role of hypoxia in PRMT activation in A549 human lung epithelial cells, as well as the role of ischemia in PRMT activation in the lung of miniature pigs. In A459 cells, hypoxia increased the expression of PRMT1 and PRMT5, and overexpression of PRMT1 and PRMT5 induced apoptosis. The transfection of PRMT1 and PRMT5 small interfering RNA (siRNA) prevented hypoxia-inducible factor (HIF)-1α expression and apoptosis in A549 cells. Hypoxia-induced expression of PRMT1 and PRMT5 was blocked by p38 and JNK mitogen-activated protein kinase (MAPK) inhibitors, but not by an inhibitor of extracellular signal-regulated kinases (ERK) 1/2. In the lungs of miniature pigs, ischemia stimulated PRMT1 and PRMT5 expression and induced phosphorylation of p38 MAPK (p-p38), phosphorylation of JNK (p-JNK), and apoptotic molecules. These results demonstrate that PRMT1 and PRMT5 are involved in hypoxia and ischemia-induced apoptosis via p-p38 MAPK and p-JNK in in vitro and in vivo models.

Fecal microbiome in dogs with lymphoid and nonlymphoid tumors.

BACKGROUND: The association of gut microbiota with cancer etiology and prognosis has been demonstrated in humans and rodents but has not been studied in dogs with different types of tumors. HYPOTHESIS/OBJECTIVES: To analyze microbiome composition according to tumor progression based on metastasis, recurrence, and therapeutic response in canine tumors. ANIMALS: Thirty-two client-owned dogs were divided into 3 groups: healthy (n = 9), with lymphoma (n = 12), with nonlymphoid tumors (n = 11). METHODS: Retrospective case series included animals were divided into subgroups according to the nature and severity of their tumors. Feces were screened for the 16S rRNA gene. RESULTS: Overall, alpha diversity was significantly reduced in dogs with tumors (n = 23; 12 lymphoid and 11 nonlymphoid) compared to healthy dogs (n = 9). Bacteroides had lower abundance in canine tumors at genus level. Staphylococcus showed significantly reduced abundance in dogs with aggressive tumor progression. Higher white blood cell (WBC) and neutrophil counts and lower hematocrit were significant in dogs with aggressive tumor. Spearman's rank correlation coefficient analysis revealed several measurements that showed moderate to strong correlations, including Coprococcus with total WBC count, neutrophil count, and hematocrit in the aggressive tumor group, and Saccharimonas with serum albumin and sodium concentration in all tumor dogs. CONCLUSION AND CLINICAL IMPORTANCE: The diversity of the gut microbiome was significantly reduced in dogs with tumors compared to healthy dogs. Correlations were found between changes in blood measurements and changes in microbiome composition in relation to paraneoplastic syndrome.

Monitoring mRNA Expression Patterns in Macrophages in Response to Two Different Strains of Probiotics.

As an initial study to elucidate the molecular mechanism of how probiotics modulate macrophage activity, we monitored mRNA expression patterns in peritoneal macrophages (PMs) treated with two different strains of probiotics. After treatment with either Weissella cibaria WIKIM28 or Latilactobacillus sakei WIKIM50, total RNAs from PMs were isolated and subjected into gene chip analyses. As controls, mRNAs from vehicle (phosphate-buffered saline, PBS)-treated PMs were also subjected to gene chip analysis. Compared to vehicle (PBS)-treated PMs, WIKIM28-treated and WIKIM50-treated PMs exhibited a total of 889 and 432 differentially expressed genes with expression differences of at least 4 folds, respectively. Compared to WIKIM28-treated PMs, WIKIM50-treated PMs showed 25 up-regulated genes and 21 down-regulated genes with expression differences of more than 2 folds. Interestingly, mRNA transcripts of M2 macrophage polarization marker such as anxa1, mafb, and sepp1 were increased in WIKIM50-treated PMs comparing to those in WIKIM28-treated PMs. Reversely, mRNA transcripts of M1 macrophage polarization marker such as hdac9, ptgs2, and socs3 were decreased in WIKIM50-treated PMs comparing to those in WIKIM28-treated PMs. In agreement with these observations, mRNA expression levels of tumor necrosis factor-α and interleukin-1α were significantly reduced in WIKIM50-treated macrophages compared to those in WIKIM28-treated macrophages. These results may indicate that probiotics can be classified as two different types depending on their ability to convert macrophages into M1 or M2 polarization.

Complete genome sequence of probiotic Lactobacillus johnsonii 7409N31 isolated from a healthy Hanwoo calf.

Lactobacillus johnsonii 7409N31 was isolated from the feces of a healthy 11-day-old Hanwoo calf from a farm in Geochang-gun, Gyeongsangnam-do, Korea. The genome of the strain was completely sequenced using the PacBio RSII sequencing system, and it was confirmed that it was composed of one circular chromosome. The size of the entire genome was 2,198,442 bp, and it had 35.01 mol% guanine + cytosine (G + C) content and 2,222 protein-coding sequences, 24 rRNA, 3 ncRNA, and 112 tRNA genes. Strain 7409N31 possessed genes encoding enzymes involved in the hydrolysis of both fibrous and non-fibrous carbohydrates. These data provide a comprehensive theoretical understanding for developing industrial probiotic feed additives that improve nutrient digestibility.

Hyperglycemia induces apoptosis via CB1 activation through the decrease of FAAH 1 in retinal pigment epithelial cells.

Fatty acid amide hydrolase (FAAH), the enzyme responsible for the degradation of the main endocannabinoid, anandamide, and related fatty acid amides, has emerged as a regulator of endocannabinoid signaling. Retinal pigment epithelial (RPE) cells are believed to be important cells in the pathogenesis of diabetic retinopathy. However, the pathophysiology of FAAH in diabetic retinopathy has not been determined. Thus, we examined the effect of high glucose (HG) on the expression of FAAH and CB(1)R in the ARPE-19 human RPE cells. We found that HG downregulated the expression of FAAH 1 mRNA and protein in ARPE-19 cells. In contrast, it upregulated the expression of CB(1)R mRNA and protein. HG-induced internalization of CB(1)R in HEK 293 cells and ARPE-19 cells was blocked by overexpression of FAAH 1 and treatment with the CB(1)R blocker, AM 251. HG-induced generation of reactive oxygen species and lipid peroxide formation were blocked by the overexpression of FAAH 1. FAAH 1 overexpression also blocked HG-induced expression of CB(1)R in the cytosolic fraction. We also investigated whether the overexpression of FAAH 1 protected against HG-induced apoptosis. High glucose increased the Bax/Bcl-2 ratio and levels of cleaved PARP, cleaved caspase-9 and caspase-3, and reduced cell viability. HG-induced apoptotic effects were reduced by the overexpression of FAAH 1, treatment with the CB(1)R-specific antagonist AM 251 and CB(1)R siRNA transfection. In conclusion, HG-induced apoptosis in ARPE-19 cells by inducing CB(1)R expression through the downregulation of FAAH 1 expression. Our results provide evidence that CB(1)R blockade through the recovery of FAAH 1 expression may be a potential anti-diabetic therapy for the treatment of diabetic retinopathy.

Lactic Acid Bacteria Strains Used as Starters for Kimchi Fermentation Protect the Disruption of Tight Junctions in the Caco-2 Cell Monolayer Model.

In this study, we investigated the effect of lactic acid bacteria (LAB) strains used as starters for kimchi fermentation, namely Lactococcus lactis WiKim0124, Companilactobacillus allii WiKim39, Leuconostoc mesenteroides WiKim0121 Leuconostoc mesenteroides WiKim33, and Leuconostoc mesenteroides WiKim32, on the intestinal epithelial tight junctions (TJs). These LAB strains were not cytotoxic to Caco-2 cells at 500 µg/ml concentration. In addition, hydrogen peroxide (H2O2) decreased Caco-2 viability, but the LAB strains protected the cells against H2O2-induced cytotoxicity. We also found that lipopolysaccharide (LPS) promoted Caco-2 proliferation; however, no specific changes were observed upon treatment with LAB strains and LPS. Our evaluation of the permeability in the Caco-2 monolayer model confirmed its increase by both LPS and H2O2. The LAB strains inhibited the increase in permeability by protecting TJs, which we evaluated by measuring TJ proteins such as zonula occludens-1 and occludin, and analyzing them by western blotting and immunofluorescence staining. Our findings show that LAB strains used for kimchi fermentation can suppress the increase in intestinal permeability due to LPS and H2O2 by protecting TJs. Therefore, these results suggest the possibility of enhancing the functionality of kimchi through its fermentation using functional LAB strains.

Kimchi intake alleviates obesity-induced neuroinflammation by modulating the gut-brain axis.

A high-fat diet (HFD) induces low-grade, chronic inflammation throughout the body including the hypothalamus, a key brain region involved in the control of satiety and energy expenditure in central nervous system (CNS). Kimchi is a traditional fermented Korean food, which is recognized as a healthy food. In this study, we evaluated its ability to suppress the obesity-induced inflammation in mice fed an HFD. Male C57BL/6 mice were fed an HFD or HFD with kimchi (pH 5.2 âˆ¼ 5.8). Oral administration of kimchi significantly reduced the body weight, fat mass gain, and levels of pro-inflammatory cytokines in serum. Furthermore, kimchi diminished the HFD-induced activation of astrocyte and microglial cells (reactive gliosis, a hallmark of CNS injury and inflammation) in hypothalamus region. IgG accumulation assay showed that kimchi ingestion suppressed HFD-induced breakage of the blood brain barrier (BBB) via upregulating the expression of tight junction molecules in cerebrovascular endothelial cells. In addition, kimchi modulated gut microbiome profiles, which showed an increase in the abundance of Akkermansia muciniphila. Moreover, kimchi enhanced acetate level and BBB integrity in A. muciniphila-colonized gnotobiotic mice. These results suggest that kimchi may exert beneficial effects to prevent and ameliorate obesity and associated neuroinflammation by changing gut microbiota composition and short-chain fatty acids production.

Probiotic Lactobacilli ameliorate alcohol-induced hepatic damage via gut microbial alteration.

Alcoholic liver disease (ALD), which includes fatty liver, cirrhosis, steatosis, fibrosis, and hepatocellular carcinoma, is a global health problem. The probiotic effects of lactic acid bacteria (LAB) are well-known; however, their protective effect against ALD remains unclear. Therefore, in this study, our objective was to assess the protective effects of LAB on ALD. To this end, mice were fed either a normal diet or an alcohol diet for 10 days (to induce ALD) accompanied by vehicle treatment (the NC and AC groups) or kimchi-derived LAB (Lactiplantibacillus plantarum DSR J266 and Levilactobacillus brevis DSR J301, the AL group; or Lacticaseibacillus rhamnosus GG, the AG group). Our results showed that mice in the AC group showed significantly higher serum aspartate aminotransferase and alanine aminotransferase levels than those in the normal diet groups; however, their levels in the AL and AG groups were relatively lower. We also observed that the AL and AG groups showed relatively lower interleukin-6 levels than the AC group. Additionally, AC group showed the accumulation of several fat vesicles in the liver, while the AL and AG groups showed remarkably lower numbers of fat vesicles. The relative abundance of Enterococcus feacalis, which showed association with liver injury, significantly increased in the AC group compared with its levels in the normal diet groups. However, the AG group showed a decreased relative abundance in this regard, confirming that LAB exerted an improvement effect on gut microbial community. These findings suggested that via gut microbiota alteration, the ingestion of LAB can alleviate the ill effects of alcohol consumption, including inflammation, liver damage, gut dysbiosis, and abnormal intestinal nutrient metabolism.

Cannabinoid receptor 1 mediates high glucose-induced apoptosis via endoplasmic reticulum stress in primary cultured rat mesangial cells.

The endocannabinoid system in animals and humans is involved in the onset of diverse diseases, including obesity and diabetic nephropathy, which is a major end-stage renal disease characterized by high glucose (HG)-induced apoptosis of mesangial cells. Endocannabinoids induce physiological and behavioral effects by activating two specific receptors, cannabinoid receptor 1 (CB(1)R) and cannabinoid receptor 2 (CB(2)R). However, the pathophysiology of CB(1)R in diabetic nephropathy has not been elucidated. We investigated the effects of HG on CB(1)R expression and its signaling pathways in primary cultured rat mesangial cells. HG significantly increased CB(1)R mRNA and protein levels in a time-dependent manner and induced CB(1)R internalization. NF-κB and cPLA(2) were involved in the HG-induced increase in CB(1)R levels. Using a CB(1)R antagonist (AM251) and CB(1) siRNA transfection, we showed that HG-induced CB(1)R is linked to apoptosis. Specifically, HG inhibited the expression of GRP78, but induced increases in endoplasmic reticulum (ER) stress proteins, including phosphorylated (p)-protein kinase-like ER-associated kinase, p-eukaryotic initiation factor 2α, p-activating transcription factor-4, and C/EBP homologous protein. In addition, HG increased the Bax/Bcl-2 ratio and increased the amounts of cleaved poly(ADP-ribose) polymerase and caspase-3. These apoptotic effects were prevented by AM251 and by the downregulation of CB(1)R expression by small interfering RNA. We propose a mechanism by which blockade of CB(1)R attenuates HG-induced apoptosis in rat mesangial cells. Our findings suggest that blockade of CB(1)R may be a potential therapy in diabetic nephropathy.

Salicibibacter cibarius sp. nov. and Salicibibacter cibi sp. nov., two novel species of the family Bacillaceae isolated from kimchi.

To date, all species in the genus Salicibibacter have been isolated in Korean commercial kimchi. We aimed to describe the taxonomic characteristics of two strains, NKC5-3T and NKC21-4T, isolated from commercial kimchi collected from various regions in the Republic of Korea. Cells of these strains were rod-shaped, Gram-positive, aerobic, oxidase- and catalase-positive, non-motile, halophilic, and alkalitolerant. Both strains, unlike other species of the genus Salicibibacter, could not grow without NaCl. Strains NKC5-3T and NKC21-4T could tolerate up to 25.0% (w/v) NaCl (optimum 10%) and grow at pH 7.0-10.0 (optimum 8.5) and 8.0-9.0 (optimum 8.5), respectively; they showed 97.1% 16S rRNA gene sequence similarity to each other and were most closely related to S. kimchii NKC1-1T (97.0% and 96.8% similarity, respectively). The genome of strain NKC5-3T was nearly 4.6 Mb in size, with 4,456 protein-coding sequences (CDSs), whereas NKC21-4T genome was nearly 3.9 Mb in size, with 3,717 CDSs. OrthoANI values between the novel strains and S. kimchii NKC1-1T were far lower than the species demarcation threshold. NKC5-3T and NKC21-4T clustered together to form branches that were distinct from the other Salicibibacter species. The major fatty acids in these strains were anteiso-C15:0 and anteiso-C17:0, and the predominant menaquinone was menaquinone-7. The polar lipids of NKC5-3T included diphosphatidylglycerol (DPG), phosphatidylglycerol (PG), and five unidentified phospholipids (PL), and those of NKC21-4T included DPG, PG, seven unidentified PLs, and an unidentified lipid. Both isolates had DPG, which is the first case in the genus Salicibibacter. The genomic G + C content of strains NKC5-3T and NKC21-4T was 44.7 and 44.9 mol%, respectively. Based on phenotypic, genomic, phylogenetic, and chemotaxonomic analyses, strains NKC5-3T (= KACC 22040T = DSM 111417T) and NKC21-4T (= KACC 22041T = DSM 111418T) represent two novel species of the genus Salicibibacter, for which the names Salicibibacter cibarius sp. nov. and Salicibibacter cibi sp. nov. are proposed.

Complete genome sequence of Lactobacillus amylovorus 1394N20, a potential probiotic strain, isolated from a Hanwoo calf.

Lactobacillus amylovorus are known to exist in the intestinal flora of healthy cattle or pigs. The L. amylovorus strain 1394N20 was isolated from the feces of the Hanwoo calf (Bos taurus coreanae). The genome of strain 1394N20 consists of a single circular chromosome (2,176,326 bp) with overall guanine + cytosine content of 37.8 mol%. Moreover, 2,281 protein-coding sequences, 15 rRNAs, and 65 tRNAs genes were identified in the chromosome based on the results of annotation. The bacterium has a gene encoding endoglucanase, an enzyme that hydrolyzes the 1,4-ß-D-glycosidic linkages in cellulose, hemicellulose, lichenin, and cereal ß-D-glucans. Genomic sequencing of L. amylovorus strain 1394N20 reveals the immense potential of the strain as a probiotic with nutrient digestibility.

Oral Administration of Live and Dead Cells of Lactobacillus sakei proBio65 Alleviated Atopic Dermatitis in Children and Adolescents: a Randomized, Double-Blind, and Placebo-Controlled Study.

Several studies suggest that probiotics might be useful in the management of atopic dermatitis (AD). However, the efficacy and comparison between both the administration of viable and non-viable probiotics on alleviation of AD is not well studied. Therefore, the purpose of this study was to evaluate the effect of L. sakei proBio65 live and dead cells when administered (1 × 1010 cells/day) for 12 weeks to children and adolescents (aged 3 to 18) with atopic dermatitis. In this randomized double-blind, placebo-controlled study, ninety patients were recruited and randomly allocated to either the L. sakei proBio65 live cells, L. sakei proBio65 dead cells, or placebo groups. Assessment of efficacy was based on the change in SCORing Atopic Dermatitis (SCORAD) score, Investigators Global Assessment (IGA) score, serum inflammatory markers such as the serum eosinophil (count), IgE, eosinophil cationic protein (ECP), CCL17 (thymus and activation-regulated chemokine [TARC]), and CCL27 (cutaneous T cell-attracting chemokine [CTACK]), and changes in skin condition (moisture and sebum) at baseline, week 6 and week 12. The SCORAD total score decreased in the live cells (p = 0.0015) and dead cell group (p = 0.0017) from the baseline after 12 weeks, whereas there were no significant changes in the placebo group when compared with baseline. The skin sebum content increased in both the live cell (p < 0.0001) and the dead cell group (p < 0.0001), suggesting potential improvements in skin barrier functions. Current data suggested a positive improvement in alleviation of AD symptoms upon oral administration of L. sakei proBio65 in both viable and non-viable forms.

Latilactobacillus sakei WIKIM31 Decelerates Weight Gain in High-Fat Diet-Induced Obese Mice by Modulating Lipid Metabolism and Suppressing Inflammation.

Obesity and related metabolic diseases are major problems worldwide. Some probiotics are currently considered potential therapeutic strategies for obesity. We aimed to investigate the antiobesity efficacy of Latilactobacillus sakei WIKIM31 in obese mice induced by a high fat diet. The administration of a high-fat diet with L. sakei WIKIM31 reduced body weight gain, epididymal fat mass, triglyceride and total cholesterol levels in the blood, and remarkably decreased the expression of lipogenesis-related genes in the epididymal adipose tissue and liver. Interestingly, intake of L. sakei WIKIM31 improved gut barrier function by increasing the gene expression of tight junction proteins and suppressing the inflammatory responses. Additionally, L. sakei WIKIM31 enhanced the production of short-chain fatty acids, such as butyrate and propionate, in the intestinal tract. These results showed that L. sakei WIKIM31 can be used as a potential therapeutic probiotic for obesity.

Lentibacillus cibarius sp. nov., isolated from kimchi, a Korean fermented food.

Two bacterial strains designated NKC220-2T and NKC851-2 were isolated from commercial kimchi from different areas in Korea. The strains were Gram-positive, aerobic, oxidaseand catalase-positive, rod-shaped, spore-forming, non-motile, and halophilic bacteria. Both strains grew without NaCl, unlike type species in the genus Lentibacillus. The optimal pH for growth was 8.0, higher than that of the type species in the genus Lentibacillus, although growth was observed at pH 5.5-9.0. 16S rRNA gene sequence-based phylogenetic analysis indicated that the two strains (99.3-99.9% similarity) are grouped within the genus Lentibacillus and most closely related to Lentibacillus juripiscarius IS40-3T (97.4-97.6% similarity) isolated from fish sauce in Thailand. OrthoANI value between two novel strains and Lentibacillus lipolyticus SSKP1-9T (79.5-79.6% similarity) was far lower than the species demarcation threshold. Comparative genomic analysis displayed differences between the two strains as well as among other strains belonging to Lentibacillus. Furthermore, each isolate had strain-specific groups of orthologous genes based on pangenome analysis. Genomic G + C contents of strains NKC-220-2T and NKC851-2 were 41.9 and 42.2 mol%, respectively. The strains contained meso-diaminopimelic acid in their cell walls, and the major menaquinone was menaquinone-7. Phosphatidylglycerol, diphosphatidylglycerol, and an unidentified glycolipid, aminophospholipid, and phospholipid were the major polar lipid components of both strains. The major cellular fatty acids of the strains were anteiso-C15:0 and anteiso-C17:0. Based on phenotypic, genomic, phylogenetic, and chemotaxonomic features, strains NKC220-2T and NKC851-2 represent novel species of the genus Lentibacillus, for which the name Lentibacillus cibarius sp. nov. is proposed. The type strain is NKC220-2T (= KACC 21232T = JCM 33390T).