Mutanolysin-Digested Peptidoglycan of Lactobacillus reuteri Promotes the Inhibition of Porphyromonas gingivalis Lipopolysaccharide-Induced Inflammatory Responses through the Regulation of Signaling Cascades via TLR4 Suppression.

Periodontitis is an oral infectious disease caused by various pathogenic bacteria, such as Porphyromonas gingivalis. Although probiotics and their cellular components have demonstrated positive effects on periodontitis, the beneficial impact of peptidoglycan (PGN) from probiotic Lactobacillus remains unclear. Therefore, our study sought to investigate the inhibitory effect of PGN isolated from L. reuteri (LrPGN) on P. gingivalis-induced inflammatory responses. Pretreatment with LrPGN significantly inhibited the production of interleukin (IL)-1ß, IL-6, and CCL20 in RAW 264.7 cells induced by P. gingivalis lipopolysaccharide (LPS). LrPGN reduced the phosphorylation of PI3K/Akt and MAPKs, as well as NF-κB activation, which were induced by P. gingivalis LPS. Furthermore, LrPGN dose-dependently reduced the expression of Toll-like receptor 4 (TLR4), indicating that LrPGN inhibits periodontal inflammation by regulating cellular signaling cascades through TLR4 suppression. Notably, LrPGN exhibited stronger inhibition of P. gingivalis LPS-induced production of inflammatory mediators compared to insoluble LrPGN and proteinase K-treated LrPGN. Moreover, MDP, a minimal bioactive PGN motif, also dose-dependently inhibited P. gingivalis LPS-induced inflammatory mediators, suggesting that MDP-like molecules present in the LrPGN structure may play a crucial role in the inhibition of inflammatory responses. Collectively, these findings suggest that LrPGN can mitigate periodontal inflammation and could be a useful agent for the prevention and treatment of periodontitis.

Whey fermented by Enterococcus faecalis M157 exhibits antiinflammatory and antibiofilm activities against oral pathogenic bacteria.

The aim of the present study was to investigate the antiinflammatory and antibiofilm effects of whey fermented by Enterococcus faecalis M157 (M157-W) against oral pathogenic bacteria. The M157-W significantly inhibited IL-1ß, IL-6, and nitric oxide induced by the lipopolysaccharide of Porphyromonas gingivalis in RAW 264.7 cells. The M157-W also inhibited the production of IL-1ß and IL-8 in human periodontal ligament cells. Treatment with M157-W suppressed the phosphorylation of mitogen-activated protein kinases as well as the activation of nuclear factor-κB in RAW 264.7 cells stimulated by P. gingivalis lipopolysaccharide. Furthermore, M157-W dose-dependently inhibited Streptococcus mutans biofilm, whereas unfermented whey did not inhibit the biofilm. Treatment with M157-W significantly suppressed gtfB, gtfC, and gtfD gene expression in S. mutans compared with the control (0 µg/mL), indicating that M157-W inhibits S. mutans biofilm formation by reducing the synthesis of extracellular polymeric substances. Collectively, these results suggest that M157-W has antiinflammatory and antibiofilm activities against oral pathogenic bacteria.

Inhibitory Effect of Bacterial Lysates Extracted from Pediococcus acidilactici on the Differentiation of 3T3-L1 Pre-Adipocytes.

Postbiotics, including bacterial lysates, are considered alternatives to probiotics. The aim of the current study was to investigate the effect of bacterial lysates (BLs) extracted from Pediococcus acidilactici K10 (K10 BL) and P. acidilactici HW01 (HW01 BL) on the differentiation of 3T3-L1 pre-adipocytes. Both K10 and HW01 BLs significantly reduced the accumulation of lipid droplets and the amounts of cellular glycerides in 3T3-L1 cells (p < 0.05). However, another postbiotic molecule, peptidoglycan of P. acidilactici K10 and P. acidilactici HW01, moderately inhibited the accumulation of lipid droplets, whereas heat-killed P. acidilactici did not effectively inhibit the lipid accumulation. The mRNA and protein levels of the transcription factors, peroxisome proliferator-activated receptor γ and CCAAT/enhancer-binding protein α, responsible for the differentiation of 3T3-L1 cells, were significantly inhibited by K10 BL and HW01 BL (p < 0.05). Both K10 and HW01 BLs decreased adipocyte-related molecules, adipocyte fatty acid-binding protein and lipoprotein lipase, at the mRNA and protein levels. Furthermore, both K10 and HW01 BLs also downregulated the mRNA expression of leptin, but not resistin. Taken together, these results suggest that P. acidilactici BLs mediate anti-adipogenic effects by inhibiting adipogenic-related transcription factors and their target molecules.

Biotransformation of whey by Weissella cibaria suppresses 3T3-L1 adipocyte differentiation.

Biotransformation, the structural modification of chemical compounds, has proved to be an indispensable tool in providing beneficial health effects. Although the health benefits of biotransformation using plant sources has been widely studied, the anti-adipogenic effect of biotransformed dairy products, such as whey, have not yet been demonstrated. Here, we investigated the anti-adipogenic effect of whey biotransformed by Weissella cibaria in 3T3-L1 adipocytes. Weissella cibaria-biotransformed whey considerably reduced the accumulation of lipid droplets and intracellular triglycerides in 3T3-L1 cells. In the presence of W. cibaria-biotransformed whey, the mRNA and protein expression of a key transcription factor, peroxisome proliferator-activated receptor γ (PPARγ), for adipogenesis was markedly suppressed in 3T3-L1 cells. Additionally, W. cibaria-biotransformed whey also decreased the mRNA and protein expressions of lipoprotein lipase and adipocyte fatty acid-binding protein, which are regulated by PPARγ. Moreover, W. cibaria-biotransformed whey inhibited the expression of adipokines, resistin, and leptin. Collectively, these results suggest that whey biotransformed by W. cibaria has the potential to exert anti-adipogenic effects by inhibiting intracellular signaling events of adipogenic-related transcription factors and target genes.

In Vitro Antibiofilm and Anti-Inflammatory Properties of Bacteriocins Produced by Pediococcus acidilactici Against Enterococcus faecalis.

Although Enterococcus faecalis is known as a commensal microorganism in the gastrointestinal tract, it is linked to various foodborne infections. In addition, biofilm formation in E. faecalis is associated with the infections by exacerbating inflammation. Hence, we demonstrated that bacteriocins produced by Pediococcus acidilactici exhibited antibiofilm and anti-inflammatory activities against E. faecalis. Bacteriocins of P. acidilactici K10 and HW01 strains significantly reduced biofilm formation by E. faecalis on surfaces of polystyrene (p < 0.005 and p < 0.01 at 24 h, respectively) and stainless steel (p < 0.005 and p < 0.01 at 72 h, respectively), while both bacteriocins did not effectively reduce the growth of E. faecalis planktonic cells. Moreover, extracellular polymeric substances (EPSs) produced by E. faecalis were substantially decreased in the presence of P. acidilactici bacteriocin (p < 0.005), suggesting that E. faecalis biofilm formation was reduced by decreasing the production of EPSs, but not by killing bacteria. The bacteriocin of P. acidilactici also reduced the adhesion of E. faecalis to human intestinal epithelial cells (p < 0.005). Furthermore, both bacteriocins significantly inhibited E. faecalis-induced interleukin-8 production in human intestinal epithelial cells (p < 0.01 for K10 bacteriocin and p < 0.005 for HW01 bacteriocin). These results suggest that the bacteriocin of P. acidilactici can eradicate E. faecalis biofilms and inhibit the E. faecalis-induced inflammatory response in intestinal epithelial cells.

Different dietary fibre sources and risks of colorectal cancer and adenoma: a dose-response meta-analysis of prospective studies.

Dietary fibre is believed to provide important health benefits including protection from colorectal cancer. However, the evidence on the relationships with different dietary fibre sources is mixed and little is known about which fibre source provides the greatest benefits. We conducted a dose-response meta-analysis of prospective cohorts to summarise the relationships of different fibre sources with colorectal cancer and adenoma risks. Analyses were restricted to publications that reported all fibre sources (cereals, vegetables, fruits, legumes) to increase comparability between results. PubMed and Embase were searched through August 2018 to identify relevant studies. The summary relative risks (RR) and 95 % CI were estimated using a random-effects model. This analysis included a total of ten prospective studies. The summary RR of colorectal cancer associated with each 10 g/d increase in fibre intake were 0·91 (95 % CI 0·82, 1·00; I2 = 0 %) for cereal fibre, 0·95 (95 % CI 0·87, 1·03, I2 = 0 %) for vegetable fibre, 0·91 (95 % CI 0·78, 1·06, I2 = 43 %) for fruit fibre and 0·84 (95 % CI 0·63, 1·13, I2 = 45 %) for legume fibre. For cereal fibre, the association with colorectal cancer risk remained statistically significant after adjustment for folate intake (RR 0·89, 95 % CI 0·80, 0·99, I2 = 2 %). For vegetable and fruit fibres, the dose-response curve suggested evidence of non-linearity. All fibre sources were inversely associated with incident adenoma (per 10 g/d increase: RR 0·81 (95 % CI 0·54, 1·21) cereals, 0·84 (95 % CI 0·71, 0·98) for vegetables, 0·78 (95 % CI 0·65, 0·93) for fruits) but not associated with recurrent adenoma. Our data suggest that, although all fibre sources may provide some benefits, the evidence for colorectal cancer prevention is strongest for fibre from cereals/grains.

Orally administered collagen peptide protects against UVB-induced skin aging through the absorption of dipeptide forms, Gly-Pro and Pro-Hyp.

Collagen hydrolysate is a well-known nutritional supplement for the improvement of healthy skin. Here, collagen peptide NS (CPNS) from fish scale was prepared, and its physicochemical properties were investigated. Gly-Pro was revealed as a representative low molecular weight peptide of CPNS, by performing prep-HPLC and LC-MS/MS. CPNS treatment attenuated matrix metalloproteinase-1 production and increased the synthesis of type 1 procollagen in HDF cells. After orally administering CPNS to rats, the plasma concentrations of Gly-Pro and Pro-Hyp increased dramatically. To examine the protective effects of CPNS against ultraviolet B (UVB)-induced photoaging in vivo, the dorsal skins of hairless mice were exposed to UVB and supplemented with CPNS for 12 weeks. The CPNS consumption significantly attenuated UVB-induced wrinkle formation, transepidermal water loss, and epidermis thickness, and increased skin hydration. Collectively, these results suggest that bioactive peptides of CPNS, Gly-Pro and Pro-Hyp, exert beneficial effects on skin health.

Staphylococcus aureus lipoproteins augment inflammatory responses in poly I:C-primed macrophages.

Secondary bacterial infection contributes to severe inflammation following viral infection. Among foodborne pathogenic bacteria, Staphylococcus aureus is known to exacerbate severe inflammatory responses after infection with single-stranded RNA viruses such as influenza viruses. However, it has not been determined if S. aureus infection enhances inflammatory responses after infection with RNA enteric viruses, including rotavirus, which is a double-stranded RNA virus. We therefore investigated the molecular mechanisms by which a cell wall component of S. aureus enhanced inflammatory responses during enteric viral infection using poly I:C-primed macrophages, which is a well-established model for double-stranded RNA virus infection. S. aureus lipoproteins enhanced IL-6 as well as TNF-α production in poly I:C-primed macrophages. Pam2CSK4, a mimic of Gram-positive bacterial lipoproteins and S. aureus lipoproteins, also significantly enhanced IL-6 production in poly I:C-primed macrophages. While IFN-ß expression was increased in poly I:C-primed macrophages treated with Pam2CSK4 or S. aureus lipoproteins, the level of IL-6 enhancement in poly I:C-primed macrophages was decreased in the presence of anti-IFN-α/ß receptor antibody, suggesting that IFN-ß plays an important role in enhanced IL-6 production. Phosphatidylinositol-3-kinase, Akt, ERK and NF-κB were also involved in the enhanced IL-6 production. Collectively, these results suggest that S. aureus lipoproteins induce excessive inflammatory responses in the presence of poly I:C.

Vibrio injenensis sp. nov., isolated from human clinical specimens.

Vibrio species are well known as motile, mostly oxidase-positive, facultative anaerobic Gram-negative bacteria. They are abundant in aquatic environments and are a common cause of human infections including diarrhea, soft tissue diseases, and bacteremia. Here, two Gram-negative bacteria, designated M12-1144T and M12-1181, were isolated from human clinical specimens and identified using a polyphasic taxonomic approach. Phylogenetic study based on 16S rRNA gene sequence analysis revealed that the isolates belong to the genus Vibrio, and are closely related to Vibrio metschnikovii KCTC 32284T (98.3%) and Vibrio cincinnatiensis KCTC 2733T (97.8%). The major fatty acids were summed feature 3 (C16:1 ω7c/C16:1 ω6c, 38.0%), C16:0 (23.0%), and summed feature 8 (C18:1 ω7c or C18:1 ω6c, 19.3%) and major polar lipids were diphosphatidylglycerol, phosphatidylglycerol, and phosphatidylethanolamine. The G + C content of the genomic DNA was determined to be 44.1 mol%. DNA-DNA relatedness between the two newly isolated strains and V. metschnikovii KCTC 32284T and V. cincinnatiensis KCTC 2733T was between 42.6 to 47.5%. The similarities of genome-to-genome distance between M12-1144T and related species ranged from 18.4-54.8%. Based on these results, a new species of the genus Vibrio, Vibrio injenensis is proposed. The type strain is M12-1144 T(=KCTC 32233T =JCM 30011T).

Enterococcus faecalis lipoteichoic acid suppresses Aggregatibacter actinomycetemcomitans lipopolysaccharide-induced IL-8 expression in human periodontal ligament cells.

Periodontitis is caused by multi-bacterial infection and Aggregatibacter actinomycetemcomitans and Enterococcus faecalis are closely associated with inflammatory periodontal diseases. Although lipopolysaccharide (LPS) of A. actinomycetemcomitans (Aa.LPS) and lipoteichoic acid of E. faecalis (Ef.LTA) are considered to be major virulence factors evoking inflammatory responses, their combinatorial effect on the induction of chemokines has not been investigated. In this study, we investigated the interaction between Aa.LPS and Ef.LTA on IL-8 expression in human periodontal ligament (PDL) cells. Aa.LPS, but not Ef.LTA, substantially induced IL-8 expression at the protein and mRNA levels. Interestingly, Ef.LTA suppressed Aa.LPS-induced IL-8 expression without affecting the binding of Aa.LPS to Toll-like receptor (TLR) 4. Ef.LTA reduced Aa.LPS-induced phosphorylation of mitogen-activated protein kinases, including ERK, JNK and p38 kinase. Furthermore, Ef.LTA inhibited the Aa.LPS-induced transcriptional activities of the activating protein 1, CCAAT/enhancer-binding protein and nuclear factor-kappa B transcription factors, all of which are known to regulate IL-8 gene expression. Ef.LTA augmented the expression of IL-1 receptor-associated kinase-M (IRAK-M), a negative regulator of TLR intracellular signaling pathways, in the presence of Aa.LPS at both the mRNA and protein levels. Small interfering RNA silencing IRAK-M reversed the attenuation of Aa.LPS-induced IL-8 expression by Ef.LTA. Collectively, these results suggest that Ef.LTA down-regulates Aa.LPS-induced IL-8 expression in human PDL cells through up-regulation of the negative regulator IRAK-M.

Clostridium kogasensis sp. nov., a novel member of the genus Clostridium, isolated from soil under a corroded gas pipeline.

Two bacterial strains, YHK0403(T) and YHK0508, isolated from soil under a corroded gas pipe line, were revealed as Gram-negative, obligately anaerobic, spore-forming and mesophilic bacteria. The cells were rod-shaped and motile by means of peritrichous flagella. Phylogenetic analysis based on 16S rRNA gene sequences indicated that the isolates were members of the genus Clostridium and were the most closely related to Clostridium scatologenes KCTC 5588(T) (95.8% sequence similarity), followed by Clostridium magnum KCTC 15177(T) (95.8%), Clostridium drakei KCTC 5440(T) (95.7%) and Clostridium tyrobutyricum KCTC 5387(T) (94.9%). The G + C contents of the isolates were 29.6 mol%. Peptidoglycan in the cell wall was of the A1γ type with meso-diaminopimelic acid. The major polar lipid was diphosphatidylglycerol (DPG), and other minor lipids were revealed as phosphatidylglycerol (PG), phosphatidylethanolamine (PE), two unknown glycolipids (GL1 and GL2), an unknown aminoglycolipid (NGL), two unknown aminophospholipids (PN1 and PN2) and four unknown phospholipids (PL1 to PL4). Predominant fatty acids were C16:0 and C16:1cis9 DMA. The major end products from glucose fermentation were identified as butyrate (12.2 mmol) and acetate (9.8 mmol). Collectively, the results from a wide range of phenotypic tests, chemotaxonomic tests, and phylogenetic analysis indicated that the two isolates represent novel species of the genus Clostridium, for which the name Clostridium kogasensis sp. nov. (type strain, YHK0403(T) = KCTC 15258(T) = JCM 18719(T)) is proposed.

Staphylococcus aureus induces IL-8 expression through its lipoproteins in the human intestinal epithelial cell, Caco-2.

Staphylococcus aureus can cause the intestinal inflammatory diseases. However, little is known about the molecular mechanism of S. aureus infection in the intestine. In the present study, we investigated whether S. aureus could stimulate human intestinal epithelial cells triggering inflammation. When the human intestinal epithelial cell-line, Caco-2, and the primary colon cells were stimulated with ethanol-inactivated S. aureus, IL-8 expression was induced in a dose-dependent manner. The inactivated S. aureus preferentially stimulated Toll-like receptor (TLR) 2 rather than TLR4. Lipoproteins, lipoteichoic acid (LTA), and peptidoglycan (PGN) are considered as potential TLR2 ligands of S. aureus. Interestingly, S aureus lipoproteins and Pam2CSK4 mimicking Gram-positive bacterial lipoproteins, but not LTA and PGN of S. aureus, significantly induced IL-8 expression in Caco-2 cells. Furthermore, lipoprotein-deficient S. aureus mutant strain failed to induce IL-8 production. Collectively, these results suggest that S. aureus stimulates the human intestinal epithelial cells to induce the chemokine IL-8 production through its lipoproteins, potentially contributing the development of intestinal inflammation.

Protein profiles in mucosal and systemic compartments in response to Vibrio cholerae in a mouse pulmonary infection model.

We have recently shown that a mouse lung infection model resulting in acute pneumonia could be used for evaluating the protective immunity induced by mucosal vaccines against Vibrio cholerae. In order to gain insight and better understanding of the pathogenicity of V. cholerae infection, we identified and compared proteins induced by V. cholerae in nasal washes, bronchoalveolar lavages (BAL), and sera. Intranasal administration of V. cholerae increased the concentration of total proteins in nasal washes and BAL fluids, but not in sera. LTQ-Orbitrap hybrid Fourier transform mass spectrometry showed that cytoskeletal proteins, protease inhibitors and anti-inflammatory mediators were present in nasal washes from uninfected mice. The distinctly expressed proteins in nasal washes in response to V. cholerae mainly consisted of protease inhibitors, anti-inflammatory proteins, and anti-microbial proteins. A number of protease inhibitors and anti-inflammatory proteins were selectively expressed in BAL fluids from V. cholerae-infected mice, while cytoskeletal proteins and heat shock proteins were mainly observed in BAL fluids from uninfected mice. A large number of serum complements, protease inhibitors, and acute phase proteins were expressed in V. cholerae-infected mice. Collectively, these results suggest that intranasal administration of V. cholerae leading to acute pneumonia elicited alterations of protein profiles associated with immune homeostasis and host protection in both the mucosal and systemic compartments.

Regulatory Effect of Spray-Dried Lactiplantibacillus plantarum K79 on the Activation of Vasodilatory Factors and Inflammatory Responses.

The reduction of nitric oxide (NO) bioavailability in the endothelium induces endothelial dysfunction, contributing to the development of hypertension. Although Lactobacillus consumption decreases blood pressure, intracellular signaling pathways related to hypertension have not been well elucidated. Thus, this study examined the effect of spray-dried Lactiplantibacillus plantarum K79 (LpK79) on NO production, intracellular signaling pathways, and inflammatory responses related to vascular function and hypertension. NO production was assessed in human umbilical vein endothelial cells (HUVECs) treated with LpK79. Endothelial NO synthase (eNOS) and intracellular signaling molecules were determined using Western blot analysis. LpK79 dose-dependently increased NO production and activated eNOS via the phosphoinositide 3-kinase/Akt signaling pathway HUVECs. Moreover, LpK79 mitigated the activation of crucial factors pivotal for vascular contraction in smooth muscle cells, such as phospholipase Cγ, myosin phosphatase target subunit 1, and Rho-associated kinase 2. When HUVECs were treated with LpL79 in the presence of Escherichia coli lipopolysaccharide (LPS), LpK79 effectively suppressed mRNA and protein expression of pro-inflammatory mediators induced by E. coli LPS. These results suggest that LpK79 provided a beneficial effect on the regulation of vascular endothelial function.

Synergistic Inhibitory Effect of Lactobacillus Cell Lysates and Butyrate on Poly I:C-Induced IL-8 Production in Human Intestinal Epithelial Cells.

Postbiotics include cell lysates (CLs), enzymes, cell wall fragments, and heat-killed bacteria derived from probiotics. Although postbiotics are increasingly being considered for their potential health-promoting properties, the effects of postbiotics on virus-mediated inflammatory responses in the intestine have not been elucidated. Hence, the present study aimed to examine whether CLs of Lactipantibacillus plantarum (LP CL) and Lacticaseibacillus rhamnosus GG (LR CL) could inhibit virus-mediated inflammatory responses in the human intestinal epithelial cell line HT-29 in vitro. Pretreatment with LP CL and LR CL significantly inhibited interleukin (IL)-8 production, which was induced by poly I:C, a synthetic analog of double-stranded RNA (dsRNA) viruses, at the mRNA and protein levels in HT-29 cells. However, peptidoglycans and heat-killed L. plantarum and L. rhamnosus GG did not effectively inhibit IL-8 production. LP CL and LR CL attenuated the poly I:C-induced phosphorylation of ERK and JNK and the activation of NF-κB, suggesting that these CLs could inhibit poly I:C-induced IL-8 production by regulating intracellular signaling pathways in HT-29 cells. Furthermore, among the short-chain fatty acids, butyrate enhanced the inhibitory effect of CLs on poly I:C-induced IL-8 production at the mRNA and protein levels in HT-29 cells, while acetate and propionate did not. Taken together, these results suggest that both LP CL and LR CL could act as potent effector molecules that can inhibit virus-mediated inflammatory responses and confer synergistic inhibitory effects with butyrate in human intestinal epithelial cells.

Inhibitory Effect of Genomic DNA Extracted from Pediococcus acidilactici on Porphyromonas gingivalis Lipopolysaccharide-Induced Inflammatory Responses.

This study aimed to assess whether genomic DNA (gDNA) extracted from Pediococcus acidilactici inhibits Porphyromonas gingivalis lipopolysaccharide (LPS)-induced inflammatory responses in RAW 264.7 cells. Pretreatment with gDNA of P. acidilactici K10 or P. acidilactici HW01 for 15 h effectively inhibited P. gingivalis LPS-induced mRNA expression of interleukin (IL)-1ß, IL-6, and monocyte chemoattractant protein (MCP)-1. Although both gDNAs did not dose-dependently inhibit P. gingivalis LPS-induced mRNA expression of IL-6 and MCP-1, they inhibited IL-1ß mRNA expression in a dose-dependent manner. Moreover, pretreatment with both gDNAs inhibited the secretion of IL-1ß, IL-6, and MCP-1. When RAW 264.7 cells were stimulated with P. gingivalis LPS alone, the phosphorylation of mitogen-activated protein kinases (MAPKs) was increased. However, the phosphorylation of MAPKs was reduced in the presence of gDNAs. Furthermore, both gDNAs restored IκBα degradation induced by P. gingivalis LPS, indicating that both gDNAs suppressed the activation of nuclear factor-κB (NF-κB). In summary, P. acidilactici gDNA could inhibit P. gingivalis LPS-induced inflammatory responses through the suppression of MAPKs and NF-κB, suggesting that P. acidilactici gDNA could be effective in preventing periodontitis.

Genomic DNA Extracted from Lactiplantibacillus plantarum Attenuates Porphyromonas gingivalis Lipopolysaccharide (LPS)-Induced Inflammatory Responses via Suppression of Toll-Like Receptor (TLR)-Mediated Mitogen-Activated Protein Kinase (MAPK) and Nuclear Factor-κB (NF-κB) Signaling Pathways.

In the present study, we aimed to examine the inhibition of genomic DNA from Lactiplantibacillus plantarum (LpDNA) on Porphyromonas gingivalis lipopolysaccharide (PgLPS)-induced inflammatory responses in RAW264.7 cells. Pretreatment with LpDNA for 15 h significantly inhibited PgLPS-induced mRNA expression and protein secretion of interleukin (IL)-1ß, IL-6, and monocyte chemoattractant protein-1. LpDNA pretreatment also reduced the mRNA expression of Toll-like receptor (TLR)2 and TLR4. Furthermore, LpDNA inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs) and the activation of nuclear factor-κB (NF-κB) induced by PgLPS. Taken together, these findings demonstrate that LpDNA attenuates PgLPS-induced inflammatory responses by regulating MAPKs and NF-κB signaling pathways through the suppression of TLR2 and TLR4 expression.

AHR rs4410790 genotype and IgG levels: Effect modification by lifestyle factors.

Inflammation is a multifaceted marker resulting from complex interactions between genetic and lifestyle factors. Emerging evidence suggests Aryl hydrocarbon receptor (AHR) protein may be implicated in the regulation of immune system and inflammatory responses. To investigate whether rs4410790 genotype (TT, TC, CC) near AHR gene is related to serum IgG levels, a marker of chronic inflammation, and whether lifestyle factors modifies the relationship, we conducted a cross-sectional study by recruiting 168 Korean adults. Participants responded to a lifestyle questionnaire and provided oral epithelial cells and blood samples for biomarker assessment. Among these participants, C allele was the minor allele, with the minor allele frequency of 40%. The rs4410790 TT genotype was significantly associated with elevated IgG levels compared with TC/CC genotypes, after adjusting for potential confounders (p = 0.04). The relationship varied significantly by levels of alcohol consumption (P interaction = 0.046) and overweight/obese status (P interaction = 0.02), but not by smoking status (P interaction = 0.64) and coffee consumption (P interaction = 0.55). Specifically, higher IgG levels associated with the TT genotype were evident in frequent drinkers and individuals with BMI≥23kg/m2, but not in their counterparts. Thus, rs4410790 genotype may be associated with IgG levels and the genetic predisposition to higher IgG levels may be mitigated by healthy lifestyle factors like infrequent drinking and healthy weight.

Pharmaceutical Importance of Some Promising Plant Species with Special Reference to the Isolation and Extraction of Bioactive Compounds: A Review.

BACKGROUND: Active principles from natural sources, in the form of extracts and natural compounds, provide an infinite number of bioactive compounds with consummate disposal of chemical diversity. These compounds and active principles are of utmost importance in the discovery of drugs of biological origin particularly, from plants. OBJECTIVES: Development of resourceful technology for the isolation and extraction of bioactive compounds of medicinal importance is considered as an important task for researchers. There are a number of extraction, isolation, and characterization techniques currently utilized; however, most are laborious and use toxic chemicals and huge quantities of raw materials with a very low output. There are a number of abiotic and biotic factors that affects the quality and the quantity of plants bioactive compounds. Considering this, the objectives of the current review are to discuss the various extraction and characterization techniques used to isolate the essential bioactive compounds from three plant species and the biotic and abiotic factors that affect the quantity and quality of the plants secondary metabolites. METHODS: Many advanced technologies have been developed and tested for extraction, characterization, and their capacity for high yield products, and those requiring less application of toxic solvents are investigated continuously. CONCLUSION: In this context, the present review summarizes the different types of extraction and characterization techniques utilized commercially by the food, drug, and pharmaceutical industries for better output and environmentally- and health-benefiting products with special reference to three industrially important plants: Leonotis leonurus (L.) R.Br. (Lamiaceae) and Santalum album L. (Santalaceae) and Aloe vera (L.) Burm. f. (Aloaceae or Asphodelaceae).

Effects of Spore-Displayed p75 Protein from Lacticaseibacillus rhamnosus GG on the Transcriptional Response of HT-29 Cells.

A Lacticaseibacillus rhamnosus GG-derived protein, p75, is one of the key molecules exhibiting probiotic activity. However, the molecular mechanism and transcriptional response of p75 in human intestinal epithelial cells are not completely understood. To gain a deeper understanding of its potential probiotic action, this study investigated genome-wide responses of HT-29 cells to stimulation by spore-displayed p75 (CotG-p75) through a transcriptome analysis based on RNA sequencing. Analysis of RNA-seq data showed significant changes of gene expression in HT-29 cells stimulated by CotG-p75 compared to the control. A total of 189 up-regulated and 314 down-regulated genes was found as differentially expressed genes. Gene ontology enrichment analysis revealed that a large number of activated genes was involved in biological processes, such as epithelial cell differentiation, development, and regulation of cell proliferation. A gene-gene interaction network analysis showed that several DEGs, including AREG, EREG, HBEGF, EPGN, FASLG, GLI2, CDKN1A, FOSL1, MYC, SERPINE1, TNFSF10, BCL6, FLG, IVL, SPRR1A, SPRR1B, SPRR3, and MUC5AC, might play a critical role in these biological processes. RNA-seq results for selected genes were verified by reverse transcription-quantitative polymerase chain reaction. Overall, these results provide extensive knowledge about the transcriptional responses of HT-29 cells to stimulation by CotG-p75. This study showed that CotG-p75 can contribute to cell survival and epithelial development in human intestinal epithelial cells.