Transcriptome-Based Analysis in Lactobacillus plantarum WCFS1 Reveals New Insights into Resveratrol Effects at System Level.

SCOPE: This study was undertaken to expand our insights into the mechanisms involved in the tolerance to resveratrol (RSV) that operate at system-level in gut microorganisms and advance knowledge on new RSV-responsive gene circuits. METHODS AND RESULTS: Whole genome transcriptional profiling was used to characterize the molecular response of Lactobacillus plantarum WCFS1 to RSV. DNA repair mechanisms were induced by RSV and responses were triggered to decrease the load of copper, a metal required for RSV-mediated DNA cleavage, and H2 S, a genotoxic gas. To counter the effects of RSV, L. plantarum strongly up- or downregulated efflux systems and ABC transporters pointing to transport control of RSV across the membrane as a key mechanism for RSV tolerance. L. plantarum also downregulated tRNAs, induced chaperones, and reprogrammed its transcriptome to tightly control ammonia levels. RSV induced a probiotic effector gene and a likely deoxycholate transporter, two functions that improve the host health status. CONCLUSION: Our data identify novel protective mechanisms involved in RSV tolerance operating at system level in a gut microbe. These insights could influence the way RSV is used for a better management of gut microbial ecosystems to obtain associated health benefits.

Korean red ginseng ameliorated experimental pancreatitis through the inhibition of hydrogen sulfide in mice.

AIM: Effective therapy to treat acute pancreatitis (AP) or to prevent its recurrence/complication is still not available. Based on previous results that suggest that: i) hydrogen sulfide (H2S) levels were significantly increased in pancreatitis and gastritis and ii) Korean red ginseng (KRG) efficiently attenuated Helicobacter pylori-associated gastritis through the suppressive actions of H2S, we hypothesized that KRG can ameliorate experimental pancreatitis through suppression of H2S generation. METHODS: C57BL/6 mice were pre-administered KRG and then subjected to cerulein injection or pancreatic duct ligation (PDL) to induce pancreatitis. Blood and pancreas tissues were collected and processed to measure serum levels of amylase, lipase and myeloperoxidase and the concentration of H2S and the levels of various inflammatory cytokine in pancreatic tissues of mice with induced AP. RESULTS: KRG significantly inhibited NaHS-induced COX-2 and TNF-α mRNA in pancreatic cells, but dl-propargylglycine did not. KRG ameliorated cerulein-induced edematous pancreatitis accompanied with significant inactivation of NF-κB and JNK in pancreatic tissues of C57BL/6 mice (p < 0.001) and also significantly ameliorated PDL-induced necrotizing pancreatitis (p<0.01); in both conditions, the significant suppression of H2S resulting from KRG pretreatment afforded rescuing outcomes. Along with suppressed levels of H2S consequent to depressed expressions of CBS and CSE mRNA, KRG administration efficiently decreased the serum level of amylase, lipase, and myeloperoxidase and the expression of inflammatory cytokines in animal models of mild or severe AP. CONCLUSIONS: These results provide evidence for the preventive and therapeutic roles of KRG against AP mediated by H2S suppression.

Short-term germ-killing effect of sugar-sweetened cinnamon chewing gum on salivary anaerobes associated with halitosis.

OBJECTIVE: The present study investigated the short-term germ-killing effect of sugar-sweetened cinnamon chewing gum on total and H2S-producing salivary anaerobes. METHODS: Fifteen healthy adult subjects were recruited in the double-blind, crossover clinical study. The three test chewing gums included: 1) sugared chewing gum containing cinnamic aldehyde and natural flavors (CinA+); 2) sugared chewing gum without cinnamic aldehyde but with natural flavors (CinA-); and 3) non-sugared chewing gum base (GB) without any flavors and without cinnamic aldehyde. A three-day "washout" period followed each treatment. Each subject chewed gum under supervision for 20 minutes at 60 chews/minute. Unstimulated whole saliva samples were collected before the subjects chewed the gum and at 20 minutes after expectoration of the gum. All saliva samples were serially diluted, plated on blood agar or agar plates that select for bacteria producing H2S, incubated anaerobically for three days, and enumerated for viable colony counts of total and H2S-producing salivary anaerobes. RESULTS: Significant reductions in total salivary anaerobes (p < 0.01) and H2S-producing salivary anaerobes (p < 0.01) were observed 20 minutes after subjects chewed the CinA+ gum. The chewing of CinA- gum also significantly reduced total salivary anaerobes (p < 0.05) and H2S-producing salivary anaerobes (p < 0.05). However, no statistically significant difference in germ-killing effect was detected between the CinA+ and CinA- gums, although there was a numeric difference. The chewing of a gum base (GB) alone did not result in a significant reduction in the total or H2S-producing salivary anaerobes (p > 0.05). CONCLUSION: The commercially available sugar-sweetened cinnamon chewing gum may benefit halitosis by reducing volatile sulfur compounds producing anaerobes in the oral cavity.

Oil field souring control by nitrate-reducing Sulfurospirillum spp. that outcompete sulfate-reducing bacteria for organic electron donors.

Nitrate injection into oil reservoirs can prevent and remediate souring, the production of hydrogen sulfide by sulfate-reducing bacteria (SRB). Nitrate stimulates nitrate-reducing, sulfide-oxidizing bacteria (NR-SOB) and heterotrophic nitrate-reducing bacteria (hNRB) that compete with SRB for degradable oil organics. Up-flow, packed-bed bioreactors inoculated with water produced from an oil field and injected with lactate, sulfate, and nitrate served as sources for isolating several NRB, including Sulfurospirillum and Thauera spp. The former coupled reduction of nitrate to nitrite and ammonia with oxidation of either lactate (hNRB activity) or sulfide (NR-SOB activity). Souring control in a bioreactor receiving 12.5 mM lactate and 6, 2, 0.75, or 0.013 mM sulfate always required injection of 10 mM nitrate, irrespective of the sulfate concentration. Community analysis revealed that at all but the lowest sulfate concentration (0.013 mM), significant SRB were present. At 0.013 mM sulfate, direct hNRB-mediated oxidation of lactate by nitrate appeared to be the dominant mechanism. The absence of significant SRB indicated that sulfur cycling does not occur at such low sulfate concentrations. The metabolically versatile Sulfurospirillum spp. were dominant when nitrate was present in the bioreactor. Analysis of cocultures of Desulfovibrio sp. strain Lac3, Lac6, or Lac15 and Sulfurospirillum sp. strain KW indicated its hNRB activity and ability to produce inhibitory concentrations of nitrite to be key factors for it to successfully outcompete oil field SRB.

A multifactorial investigation of the ability of oral health care products (OHCPs) to alleviate oral malodour.

UNLABELLED: AIM, BACKGROUND: Oral malodour (halitosis) is generally ascribable to oral microbial putrefaction generating malodorous volatile sulphur compounds which predominantly comprise dihydrogen sulphide and methyl mercaptan. This study assesses the relative effectiveness of 6 oral health care products in reducing oral cavity volatile sulphur compound concentrations. METHOD: A mixed model 3-factor factorial experimental design involving 6 volunteers, 7 treatment regimens (products I-VI* and water placebo) and 5 time-points (0.00-5.29 h) was undertaken. Electron-donating volatile sulphur compound levels were determined in triplicate using a sulphide monitor (Interscan model 1170) both prior to (0.00 h) and following oral rinsing (20 ml of 5 of the products) or chewing (2 capsules of the remaining product) episodes with each product examined (0.29, 1.29, 2.29 and 5.29 h post-administration). RESULTS: Results were recorded as peak and steady-state volatile sulphur compound equivalents (ppb). With the exception of one of the products, each oral health care product tested was found to reproducibly reduce volatile sulphur compound concentrations within 20 min of treatment; the mean % decreases in peak (and corresponding steady-state) levels ranging from 3.6 (0.0) to 16.8 (16.4)%. Subsequently, volatile sulphur compound concentrations returned to their zero-control (baseline) values within 5 h, the rate of this regression being in the reverse of the order observed for the magnitude of the primary 20 min reduction for both peak and steady-state measurements. As expected, the water placebo exerted no influence on oral cavity volatile sulphur compound levels. The most effective oral health care products contained admixtures of chlorite anion and chlorine dioxide (both of these agents have the ability to directly oxidise volatile sulphur compounds to non-malodorous products and the latter is also powerfully cidal towards odourigenic micro-organisms). CONCLUSIONS: We therefore conclude that oral health care products containing such oxohalogen oxidants may provide a useful therapeutic strategy for the treatment of oral malodour.

Modeling of the oral malodor system and methods of analysis.

Bacterial putrefaction is the central metabolic process involved in oral malodor and can easily be modeled in the salivary sediment system developed from centrifuged whole saliva. Methods used in this system for examining malodor have included measurement of (1) head space (gaseous-phase) and liquid-phase odors, organoleptically; (2) volatile sulfur compounds, by means of an electrochemical sensory instrument; (3) pH, Po2, and oxidation-reduction potential with appropriate respective electrodes; (4) the malodorous compounds indole and skatole, colorimetrically; (5) substrate levels and their effects; and (6) bacterial numbers and types. The simplicity of the system permits other analyses to be easily added, if needed, and the influence of factors and agents that affect oral malodor to be assessed. Addition of odorigenic or non-odorigenic pure cultures to the mixed bacterial flora of the system enables modification of the microflora composition and high- and low-odor-production microflora to be simulated and compared. Modeling validity has been enhanced by the use of complementary in vivo methods, such as a method used to measure the ability or potential of an oral microbial flora to produce malodor. The method involves in vivo challenge testing with cysteine, an amino acid, and measuring the hydrogen sulfide produced. Oral malodor is a multifactorial condition and models enable its systematic study and the quantitative testing of antimalodor agents.