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Our current understanding of the host-microbiota interaction in the gut is dominated by studies focused primarily on prokaryotic bacterial communities. However, there is an underappreciated symbiotic eukaryotic protistic community that is an integral part of mammalian microbiota. How commensal protozoan bacteria might interact to form a stable microbial community remains poorly understood. Here, we describe a murine protistic commensal, phylogenetically assigned as Tritrichomonas musculis, whose colonization in the gut resulted in a reduction of gut bacterial abundance and diversity in wild-type C57BL/6 mice. Meanwhile, dietary nutrient and commensal bacteria also influenced the protozoan's intestinal colonization and stability. While mice fed a normal chow diet had abundant T. musculis organisms, switching to a Western-type high-fat diet led to the diminishment of the protozoan from the gut. Supplementation of inulin as a dietary fiber to the high-fat diet partially restored the protozoan's colonization. In addition, a cocktail of broad-spectrum antibiotics rendered permissive engraftment of T. musculis even under a high-fat, low-fiber diet. Furthermore, oral administration of Bifidobacterium spp. together with dietary supplementation of inulin in the high-fat diet impacted the protozoan's intestinal engraftment in a bifidobacterial species-dependent manner. Overall, our study described an example of dietary-nutrient-dependent murine commensal protozoan-bacterium cross talk as an important modulator of the host intestinal microbiome. IMPORTANCE Like commensal bacteria, commensal protozoa are an integral part of the vertebrate intestinal microbiome. How protozoa integrate into a commensal bacterium-enriched ecosystem remains poorly studied. Here, using the murine commensal Tritrichomonas musculis as a proof of concept, we studied potential factors involved in shaping the intestinal protozoal-bacterial community. Understanding the rules by which microbes form a multispecies community is crucial to prevent or correct microbial community dysfunctions in order to promote the host's health or to treat diseases. [ABSTRACT FROM AUTHOR]

To investigate the effects of phenolic extractives on the discoloration of black locust wood (Robinia pseudoacacia) during heat treatment, phenolic compounds were extracted using an accelerated solvent extraction. The main components of the phenolic extractives were analyzed. The phenolic compounds were heat treated at 120 and 140 °C in nitrogen, oxygen, and saturated steam. The results showed that the a* values shifted toward red and the b* values shifted toward yellow after the heat treatment. The changes in the color parameters were more pronounced when the samples were treated at 140 °C in saturated steam compared with treatment at 120 °C in oxygen or nitrogen atmosphere. During heat treatment, hydroxyl groups in the phenolic components were oxidized to form carbonyl groups, or the adjacent hydroxyl groups formed quinoid structures. It was possible that the sample underwent condensation reactions to produce conjugated double-bond structures that led to the increase in color parameters. [ABSTRACT FROM AUTHOR]

Bifidobacterium longum strain JDM301, a widely used commercial strain in China, encodes at least two MazEF-like modules and one RelBE-like toxin-antitoxin (TA) system in its chromosome, designated MazE1F1 Bif, MazE2F2 Bif, and RelBEBif, respectively. Bacterial TA systems play an important role in several stress responses, but the relationship between these TA systems is largely unknown. In this study, the interactions between MazF1 Bif and MazE2 Bif or RelBBif were assessed in B. longum strain JDM301. MazF1 Bif caused the degradation of tufABif mRNA, and its toxicity was inhibited by forming a protein complex with its cognate antitoxin, MazE1 Bif. Notably, MazF1 Bif toxicity was also partially neutralized when jointly expressed with noncognate antitoxin MazE2 Bif or RelBBif. Our results show that the two noncognate antitoxins also inhibited mRNA degradation caused by MazF1 Bif toxin. Furthermore, the physical interplay between MazF1 Bif and its noncognate antitoxins was confirmed by immunoprecipitation. These results suggest that MazF1 Bif can arrest cell growth and that MazF1 Bif toxicity can be neutralized by its cognate and noncognate antitoxins. These results imply that JDM301 uses a sophisticated toxin-antitoxin interaction network to alter its physiology when coping with environmental stress. IMPORTANCE Although toxin-antitoxin (TA) systems play an important role in several stress responses, the regulatory mechanisms of multiple TA system homologs in the bacterial genome remain largely unclear. In this study, the relationships between MazE1F1 Bif and the other two TA systems of Bifidobacterium longum strain JDM301 were explored, and the interactions between MazF1 Bif and MazE2 Bif or RelBBif were characterized. In addition, the mRNA degradation activity of MazF1 Bif was demonstrated. In particular, the interaction of the toxin with noncognate antitoxins was shown, even between different TA families (MazF1 Bif toxin and RelBBif antitoxin) in JDM301. This work provides insight into the regulatory mechanisms of TA systems implicated in the stress responses of Bifidobacteria. [ABSTRACT FROM AUTHOR]

Recent progress indicates that the gut microbiota plays important role in regulating the host's glucose homeostasis. However, the mechanisms remain unclear. Here, we reported that one integral member of the murine gut microbiota, the protozoan Tritrichomonas musculis could drive the host's glucose metabolic imbalance. Using metabolomics analysis and in vivo assays, we found that mechanistically this protozoan influences the host glucose metabolism by facilitating the production of a significant amount of free choline. Free choline could be converted sequentially by choline-utilizing bacteria and then the host to a final product trimethylamine N-oxide, which promoted hepatic gluconeogenesis. Together, our data reveal a previously underappreciated gut eukaryotic microorganism by working together with other members of microbiota to influence the host's metabolism. Our study underscores the importance and prevalence of metabolic interactions between the gut microbiota and the host in modulating the host's metabolic health. [ABSTRACT FROM AUTHOR]

The physiologic signals that regulate beige adipogenesis remain incompletely understood, especially those that limit browning and prevent overexpenditure of energy. In this study, the TNF family member cytokine lymphotoxin-like inducible protein that competes with glycoprotein D for herpesvirus entry on T cells (LIGHT), also known as TNF super family protein 14 (TNFSF14), can inhibit adipose precursor differentiation into beige adipocytes. In acute cold stress, LIGHT deficiency in mice accelerated browning in the subcutaneous white adipose tissue (scWAT). Further experiments showed that LIGHT interacting with lymphotoxin-β receptor (LTβR) on adipose precursors blocked beige fat biogenesis. LTβR signals attenuated the JNK pathway, which contributed to their antibeiging effect. Blocking JNK activation using a small molecular inhibitor prevented cold-induced scWAT beiging. Furthermore, LIGHT/LTβR signals acted as an attenuator of white adipogenesis. LIGHT deficiency in mice promoted obesity during high-fat diet feeding. These findings identify the LIGHT axis as a regulator of adipose tissue homeostasis and suggest that LIGHT signaling functions as a mechanism to divert energy in favor of immune activation. [ABSTRACT FROM AUTHOR]