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Influence of short-term changes in dietary sulfur on the relative abundances of intestinal sulfate-reducing bacteria.

ABSTRACT: High-protein diets may be linked to gut inflammation due to increased production of hydrogen sulfide (H2S), a potential toxin, as an end product of microbial fermentation in the colon by sulfidogenic sulfate-reducing bacteria (SRB). We hypothesized that dietary content of sulfur-containing amino acids (SAA) leads to variation in the relative abundances of intestinal SRB, which include Desulfovibrio and Bilophila taxa. To test this hypothesis we performed a pilot crossover study in four healthy volunteers, who consumed two interventional diets for 10-14 days, containing high or low SAA content. The total energy intake was similar between the two dietary extremes. Microbial communities were characterized by 16S rRNA gene amplicon and shotgun next-generation DNA sequencing. While the relative abundance of Desulfovibrio differed among participants (ANOVA P= 0.001), we could not detect a change with dietary treatments. Similarly, no differences in Bilophila abundance were observed among individuals or dietary arms. Inter-personal differences in microbial community composition and functional gene categories differed between subjects and these differences were maintained over the course of the study. These observations are consistent with re-analysis of two previously published dietary intervention studies. Finally, we found that inter-personal differences in the taxonomic composition of fecal microbiota, including the relative abundances of SRB, were maintained over time in 19 healthy individuals in our stool donor program. These results suggest that the use of dietary interventions alone may be insufficient for rapid therapeutic targeting of SRB. Nevertheless, these pilot data provide a foundation to inform future, statistically powered, studies.

SUBMITTER: Dostal Webster A

PROVIDER: S-EPMC6748593 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Influence of short-term changes in dietary sulfur on the relative abundances of intestinal sulfate-reducing bacteria.

Dostal Webster Allison A Staley Christopher C Hamilton Matthew J MJ Huang Merry M Fryxell Kathryn K Erickson Raymond R Kabage Amanda J AJ Sadowsky Michael J MJ Khoruts Alexander A

Gut microbes 20190227 4

High-protein diets may be linked to gut inflammation due to increased production of hydrogen sulfide (H2S), a potential toxin, as an end product of microbial fermentation in the colon by sulfidogenic sulfate-reducing bacteria (SRB). We hypothesized that dietary content of sulfur-containing amino acids (SAA) leads to variation in the relative abundances of intestinal SRB, which include Desulfovibrio and Bilophila taxa. To test this hypothesis we performed a pilot crossove ...[more]

PMID: 30810441

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Project description:BackgroundDegradation of acetone by aerobic and nitrate-reducing bacteria can proceed via carboxylation to acetoacetate and subsequent thiolytic cleavage to two acetyl residues. A different strategy was identified in the sulfate-reducing bacterium Desulfococcus biacutus that involves formylation of acetone to 2-hydroxyisobutyryl-CoA.ResultsUtilization of short-chain ketones (acetone, butanone, 2-pentanone and 3-pentanone) and isopropanol by the sulfate reducer Desulfosarcina cetonica was investigated by differential proteome analyses and enzyme assays. Two-dimensional protein gel electrophoresis indicated that D. cetonica during growth with acetone expresses enzymes homologous to those described for Desulfococcus biacutus: a thiamine diphosphate (TDP)-requiring enzyme, two subunits of a B12-dependent mutase, and a NAD+-dependent dehydrogenase. Total proteomics of cell-free extracts confirmed these results and identified several additional ketone-inducible proteins. Acetone is activated, most likely mediated by the TDP-dependent enzyme, to a branched-chain CoA-ester, 2-hydroxyisobutyryl-CoA. This compound is linearized to 3-hydroxybutyryl-CoA by a coenzyme B12-dependent mutase followed by oxidation to acetoacetyl-CoA by a dehydrogenase. Proteomic analysis of isopropanol- and butanone-grown cells revealed the expression of a set of enzymes identical to that expressed during growth with acetone. Enzyme assays with cell-free extract of isopropanol- and butanone-grown cells support a B12-dependent isomerization. After growth with 2-pentanone or 3-pentanone, similar protein patterns were observed in cell-free extracts as those found after growth with acetone.ConclusionsAccording to these results, butanone and isopropanol, as well as the two pentanone isomers, are degraded by the same enzymes that are used also in acetone degradation. Our results indicate that the degradation of several short-chain ketones appears to be initiated by TDP-dependent formylation in sulfate-reducing bacteria.

Project description:BackgroundArsenic (As) toxicity is primarily based on its chemical speciation. Although inorganic and methylated As species are well characterized in terms of metabolism and formation in the human body, the origin of thiolated methylarsenicals is still unclear.ObjectivesWe sought to determine whether sulfate-reducing bacteria (SRB) from the human gut are actively involved in the thiolation of monomethylarsonic acid (MMAV).MethodsWe incubated human fecal and colon microbiota in a batch incubator and in a dynamic gut simulator with a dose of 0.5 mg MMAV in the absence or presence of sodium molybdate, an SRB inhibitor. We monitored the conversion of MMAV into monomethyl monothioarsonate (MMMTAV) and other As species by high-performance liquid chromatography coupled with inductively coupled plasma mass spectrometry analysis. We monitored the sulfate-reducing activity of the SRB by measuring hydrogen sulfide (H2S) production. We used molecular analysis to determine the dominant species of SRB responsible for As thiolation.ResultsIn the absence of sodium molybdate, the SRB activity-primarily derived from Desulfovibrio desulfuricans (piger)-was specifically and proportionally correlated (p < 0.01) to MMAV conversion into MMMTAV. Inactivating the SRB with molybdate did not result in MMAV thiolation; however, we observed that the microbiota from a dynamic gut simulator were capable of demethylating 4% of the incubated MMAV into arsenous acid (iAsIII), the trivalent and more toxic form of arsenic acid (iAsV).ConclusionWe found that SRB of human gastrointestinal origin, through their ability to produce H2S, were necessary and sufficient to induce As thiolation. The toxicological consequences of this microbial As speciation change are not yet clear. However, given the efficient epithelial absorption of thiolated methylarsenicals, we conclude that the gut microbiome-and SRB activity in particular-should be incorporated into toxicokinetic analysis carried out after As exposure.

Dataset Information

Influence of short-term changes in dietary sulfur on the relative abundances of intestinal sulfate-reducing bacteria.

Publications

Influence of short-term changes in dietary sulfur on the relative abundances of intestinal sulfate-reducing bacteria.

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