Short-Term Supplementation of Pectin Alters Substrate Dynamics and Modulates Microbial Carbohydrate Metabolism in the Gut of a Pig Model.

The interaction of pectin and gut microbiota plays an important role in maintaining animal and human health, but this interaction is not fully understood. Here, the impact of pectin supplementation on substrate dynamics and gut microbiota (in the terminal ileum and feces) was integrally investigated in a fistula pig model. Our results showed that a pectin-supplemented diet (PEC) decreased the concentrations of starch, cellulose, and butyrate in feces but not in the terminal ileum. Metagenomic sequencing revealed that PEC had a low impact on the ileal microbiota but significantly increased plant polysaccharide-degrading genera (e.g., Bacteroides, Alistipes, and Treponema) in feces. Additionally, CAZyme profiling indicated that PEC reduced GH68 and GH8 for oligosaccharide degradation in the ileal microbiome, while it enriched GH5, GH57, and GH106 for degradation of carbohydrate substrates in feces. Metabolomic analysis confirmed that PEC increased metabolites involved in carbohydrate metabolism including glucuronate and aconitate. Collectively, pectin could promote complex carbohydrate substrate degradation in the hindgut via modulating the gut microbiota.

Reduction of Redox Potential Exerts a Key Role in Modulating Gut Microbial Taxa and Function by Dietary Supplementation of Pectin in a Pig Model.

Pectin exists in a vast range of plants and has a long history of acting as a functional food additive with potential prebiotic effects on intestinal health. However, knowledge of how pectin regulates gut microbial communities is still insufficient and limited. Here, metatranscriptome sequencing revealed that a pectin-enriched diet (PEC) decreased the abundances of fungal keystone taxa (e.g., amino acid-producing Kazachstania spp.) and their genes involved in oxidative phosphorylation, while it increased the abundance of sulfate-reducing Desulfovibrio spp., and methane-producing Methanobrevibacter spp. in colon microbiomes. Furthermore, we first confirmed that PEC decreased fecal redox potential in a fistula pig model, which could be supported by the enrichment of antioxidants (e.g., inosine) in feces. Fecal metagenome analysis disclosed that certain microbial taxa promoted inosine biosynthesis from pectin degradation, including Prevotella, which plays an essential role in pectin biodegradation. Overall, these results demonstrate that pectin decreases the redox potential in pig hindgut to modulate microbial composition and functions, and specific microorganisms generate reducing agents in the course of pectin degradation to decrease redox potential of microbial ecosystem. IMPORTANCE Collective studies indicate that pectin degradation promotes extensive microorganisms that can be involved in pectin degradation directly or indirectly, or benefit from the altered physiological conditions caused by pectin ingestions. Our study focuses on effects of pectin on gut microbial taxa and functions, as well as its interactions with altered environmental features. Our results demonstrate pectin-induced proreducing shifts on colon microbial taxa and functions, and first confirm that pectin decreases hindgut redox potential, which is an important environmental feature that can modulate microbial communities. These results infer that there is bidirectional regulation between microbiota and redox potential during pectin degradation. In general, this investigation proposes new insights into the pectin-modulating gut microbial ecosystem and also provides new perspectives for targeting modulation of gut microbiota.

pH-Responsive Antimicrobial Peptide with Selective Killing Activity for Bacterial Abscess Therapy.

The unusual acidic pH of the abscess milieu is an adverse factor that decreases the therapeutic efficacy of traditional antibiotics. Moreover, avoiding both the undesired killing of commensal bacteria and the development of drug resistance remains difficult during abscess therapy. Hence, we synthesized a series of pH-responsive antimicrobial peptides equipped with efficient bacterial killing activity at pH 6.5 and inactivity at pH 7.4. Among the peptides, F5 exhibited outstanding pH-responsive antimicrobial activity and low toxicity. Fluorescence spectroscopy and electron microscopy illustrated that F5 killed bacteria via a membrane-disruptive mechanism at acidic pH values. Mouse cutaneous abscesses revealed that F5 was equipped with excellent therapeutic ability to reduce the bacterial load and cytokines without causing skin toxicity. In summary, this study reveals a strategy for selectively killing bacteria under the pathologic conditions of abscess sites while avoiding the elimination of commensal bacteria under normal physiological pH levels.