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The purpose of this paper was to study the application of a fresh preservation mode of composite film-photodynamic technology to delay the quality deterioration of Litopenaeus vannamei. Composite films (PsC and PsG) were prepared by loading curcumin and curcumin/chitosan granules, respectively, onto chitosan as the film-forming matrix. For the preservation of Litopenaeus vannamei, the photosensitive characteristics of two composite films and their mediated photodynamic sterilization (PsC-L/PsG-L) were explored. Litopenaeus vannamei was covered by PsC films and PsG films, respectively, and kept them at 4 ℃ for 0~4 days after irradiating them with a 420 nm LED light source for 10 minutes. Throughout the storage period, the preservation impact of the composite films was examined comprehensively by assessing the changes in physicochemical indicators such as total bacterial colony, volatile salt nitrogen, pH, texture, and free amino acids in Litopenaeus vannamei. Results indicated that PsG-L and PsC-L might alter the development of microorganism of Litopenaeus vannamei over a 4 day storage period. PsG-L inhibited the increase of TVB-N and pH in Litopenaeus vannamei, delayed texture softening, and had a greater preservation effect than PsC-L. Over a 2 day storage period, PsG-L treatment was more successful than PsC-L in preserving fresh amino acids and reducing the amount of bitter amino acids. Both composite films exhibit photosensitive qualities and photodynamic inhibition of freshness induced by a light source with a wavelength of 420 nm, and they effectively preserve Litopenaeus vannamei. These findings give support for the promotion and deployment of photodynamic non-thermal sterilizing technology in the preservation of aquatic products.

It is unclear how docosahexaenoic acid (DHA) improves insulin resistance via modulating gut microbiome in obese individuals. We used diet-induced obesity (DIO) mice as a model to study the effects of DHA-rich fish oil (DHA-FO) on host metabolic disorders and colonic microbiome. DHA-FO reduced fat deposition, regulated lipid profiles and alleviated insulin resistance in DIO mice. Probably because DHA-FO prevented the permeation of lipopolysaccharide across intestinal epithelial barrier, and promoted peptide YY (PYY) secretion via the mediation of short chain fatty acids receptor (FFAR2) in colon. Furthermore, DHA-FO might regulate PYY expression by reversing microbial dysbiosis, including increasing the abundance of Akkermansia muciniphila and Lactobacillus, and suppressing the growth of Helicobacter. DHA-FO also altered gut microbial function (e.g. “linoleic acid metabolism”) associated with PYY expression (r > 0.80, P

The objectives of the present study were to synthesize gliadin/tremella polysaccharide nanoparticles (Gli/TP NPs) as well as curcumin-loaded gliadin/tremella polysaccharide nanoparticles (Cur-Gli/TP NPs) and evaluate the encapsulation efficiency (EE), physicochemical stability and bioaccessibility of Cur-Gli/TP NPs. The physicochemical properties of the nanoparticles depended on the mass ratio of Gli to TP and pH values. The characterization of the Gli/TP NPs indicated that the prepared nanoparticles were the most stable when the Gli/TP mass ratio was 1:1 and pH was at 4.0–7.0. Afterward, prepared Cur-Gli/TP NPs at different pH values were studied. Compared with the EE of Cur (58.2%) in Cur-Gli NPs at pH 5.0, the EE of Cur (90.6%) in Cur-Gli/TP NPs at pH 5.0 was increased by 32.4%. Besides, the Cur-Gli/TP NPs possessed excellent physical stability, photostability, thermal stability and re-dispersibility than Cur-Gli NPs. Furthermore, the bioaccessibility of Cur reached 83.5% after encapsulation of Cur into Gli/TP NPs after in vitro digestion, indicating that Cur-Gli/TP NPs could improve curcumin bioaccessibility significantly. In summary, this study demonstrates that the new food-grade Gli/TP NPs possess high encapsulation efficiency, excellent stability and prominent nutraceutical bioaccessibility. Meanwhile, it contributes to expanding the application of TP in food-grade delivery systems.

Abstract Background The anti-inflammatory property of ω-3 polyunsaturated fatty acids (PUFA) has been exploited in the management of inflammatory bowel disease (IBD) with promising results. However, it remains unclear if PUFA play a significant role in the resolution of inflammation and promotion of mucosal healing. Krill oil (KO) is a natural product rich in PUFA and the potent antioxidant, astaxanthin. In this study, we attempted to understand the mechanisms through which KO modulates the gut microbiome and metabolome using in vitro and in vivo colitis models and a multi-omics based approach. Results KO significantly decreased LPS-induced IL1β and TNFα expression in human macrophages in vitro in a dose-dependent manner by regulating a broad spectrum of signaling pathways, including NF-κB and NOD-like receptor signaling, and displayed a synergistic effect with COX2 and IKK2 inhibitors in attenuating inflammatory pathways. Moreover, KO was involved in the resolution of inflammation by promoting M2 polarization and enhancing macrophage-mediated intracellular bacterial killing. Parasite-dependent intestinal mucosal damage and microbial dysbiosis induced by Trichuris suis infection in pigs were partially restored by feeding KO. KO supplementation reduced the abundance of Rickettsiales and several species of Lactobacillus, which were among the important features identified by random forests analysis contributing to classification accuracy for KO supplementation. Several microbial signatures with strong predictive power for the status of both infection and supplementation were identified. The inhibitory effect of KO on histidine metabolism was identified using untargeted metabolomics. KO supplementation reduced several key metabolites related to histamine metabolism by suppressing the expression of a gene encoding l-histidine decarboxylase in the colon mucosa and reducing histamine biosynthesis of microbial origin. Moreover, the pro-resolving properties of KO were validated using a Citrobacter rodentium-induced Th1-dependent colitis murine model. Further, microbial signatures with high prediction accuracy for colitis-related pathophysiological traits were identified in mice. Conclusion The findings from this study provided a mechanistic basis for optimizing microbiome-inspired alternative therapeutics in the management of IBD. The microbial signatures identified, particularly those with strong predictive accuracy for colitis phenotypes, will facilitate the development of biomarkers associated with appropriate dietary intervention to manage intestinal inflammation. Video abstract.

Alginate oligosaccharides are degradation products of alginate and have attracted increasing attention due to their versatile biological functions. In the present study, C57BL/6 mice were used to assess the ameliorative effects and mechanisms of guluronate oligosaccharides (GAOS), mannuronic oligosaccharides (MAOS), and heterozygous alginate oligosaccharides (HAOS), which are the three alginate oligosaccharides of dextran sulfate sodium (DSS)-induced ulcerative colitis. The study showed that alginate oligosaccharides alleviated pathological histological damage by slowing down weight loss, inhibiting colonic length shortening, and reducing disease activity index (DAI) and histopathological scores. Alginate oligosaccharides modulated the colonic inflammatory response by reducing colonic MPO levels and downregulating the expression of IL-6 and IL-1β. Alginate oligosaccharides reduced intestinal permeability and reversed intestinal barrier damage by increasing the number of goblet cells, decreasing LPS levels, downregulating Bax protein levels, upregulating Bcl-2 protein levels, and enhancing the expression of the E-cadherin. Furthermore, alginate oligosaccharides modulated the composition of the gut microbiota and restored the production of short-chain fatty acids (SCFAs), especially acetate and butyrate. In conclusion, our study provides a scientific basis for the role of alginate oligosaccharides in relieving ulcerative colitis.

The changes and interaction of gut microbiota, which respond to dietary supplements, play critical roles on improving human health. The modulating effect of astaxanthin on gut microbiota has been reported. However, little is known about the co-occurrence patterns among microbial taxa in response to astaxanthin. In this study, the gut microbial composition, co-occurrence patterns, and microbial correlations with physiological parameters in astaxanthin-fed normal and obese mice were studied. Astaxanthin altered the microbial composition and co-occurrence patterns in normal and obese mice. Furthermore, astaxanthin gave more profound impacts on microbiota in obesity when compared with normal mice. In group A (normal or obese mice supplemented with astaxanthin), the abundance of Acinetobacter was decreased, and Alistipes was increased by astaxanthin, which also occurred in the MA group (obese mice supplemented with astaxanthin). An operational taxonomic unit (OTU) (GreenGeneID# 4029632) assigned to the genus Bacteroides acted as a connector in the global network of A and MA groups. It may play critical roles in bridging intimate interactions between the host and other bacteria intervened by astaxanthin. Several modules correlated with physiological parameters were detected. For example, modules A12 and MA10 were significantly and negatively correlated with lipopolysaccharide (LPS) and fasting blood glucose (FBG) levels, respectively. A positive correlation was found between the node connectivity of the OTUs belonging to Clostridiaceae with LPS in obese mice, which indicated the role of Clostridiales as a potential pathological marker. Our findings provided a new interpretation of the role of astaxanthin in health and may contribute to further research on microbial community engineering.

Fucoxanthin, one of carotenoid pigments from plants and algae, is known to regulate blood glucose and insulin levels. The mechanism of its hypoglycemic activity has drawn a lot of scientific interest in recent years. In this study, we investigated the effects of fucoxanthin on intestinal glucose transport using a murine model. Our data demonstrated that fucoxanthin was able to decrease blood glucose level and alleviate insulin resistance significantly. The results from RNA-seq based transcriptomic analysis, suggested that fucoxanthin acted as a key regulator in Insulin/PI3K/AKT/mTOR signaling and PKA/AMPK/mTOR signaling pathways. Moreover, fucoxanthin ingestion resulted in a significant reduction in the protein expression of intestinal glucose transporters, such as SGLT-1, and led to decreased translocation of GLUT-2, which contributed to the regulation of blood glucose level. Together, our findings provided a mechanistic insight into the regulatory effect of fucoxanthin on blood glucose.

Abstract Chondroitin sulfate (CS) has been widely used for medical and nutraceutical purposes due to its roles in maintaining tissue structural integrity. We investigated if CS disaccharides may act as a bioactive compound and modulate gut microbial composition in mice. Our data show that CS disaccharides supplementation for 16 days significantly reduced blood LPS in the mice experiencing exhaustive exercise stress. CS disaccharides partially restored total fecal short-chain fatty acids from the level significantly repressed in mice under the stress. Our findings demonstrated that CS was likely butyrogenic and resulted in a significant increase in fecal butyrate concentration. CS disaccharides had a profound impact on gut microbial composition, affecting the abundance of 13.6% and 7.3% Operational Taxonomic Units in fecal microbial communities in healthy and stressed mice, respectively. CS disaccharides reduced the prevalence of inflammatory Proteobacteria. Together, our findings demonstrated that CS may ameliorate stress-induced intestinal inflammation. Furthermore, CS significantly increased intestinal Bacteroides acidifaciens population, indirectly exerting its immunomodulatory effect on the intestine. CS disaccharides had a significant impact on a broad range of biological pathways under stressed condition, such as ABC transporters, two-component systems, and carbohydrate metabolism. Our results will facilitate the development of CS as a bioactive nutraceutical.

Neoagarotetraose (NT), a hydrolytic product of agar by β-agarase, is known to possess bioactive properties. However, the mechanisms via which NT alleviates intestinal inflammation remain unknown. In this study, a dextran sulfate sodium (DSS)-induced murine model was developed to evaluate the effect of NT on gut microbiome and microbial metabolism using 16S rRNA gene sequencing and untargeted metabolomics. Our data demonstrate that NT ingestion improved gut integrity and inflammation scores. NT reversed the abundance of Proteobacteria from an elevated level induced by DSS and significantly increased the abundance of Verrucomicrobia. Further, NT significantly increased the abundance of Akkermansia and Lactobacillus and concomitantly decreased that of Sutterella, which were among the important features identified by random forests analysis contributing to classification accuracy for NT supplementation. A microbial signature consisting of Adlercreutzia (denominator) and Turicibacter (numerator) predicted the NT supplementation status. Moreover, NT significantly modulated multiple gut metabolites, particularly those related to histidine, polyamine and tocopherol metabolism. Together, our findings provided novel insights into the mechanisms by which NT modulated the gut microbiome and metabolome and should facilitate the development of NT as a potent prebiotic for colitis management.

Aim. To investigate the effect of light-activated hypocrellin B on the growth and membrane permeability of Gram-negative bacteria. Methods. Escherichia coli (E. coli) as a model bacterium of Gram-negative bacteria was incubated with various concentrations of hypocrellin B for 60 min and was subsequently irradiated by blue light with wavelength of 470 nm at the dose of 12 J/cm2. Colony forming units were counted and the growth inhibition rate of E. coli cells was calculated after light-activated hypocrellin B. Membrane permeability was measured using flow cytometry and confocal laser scanning microscopy (CLSM) with propidium iodide (PI) staining. Bacterial morphology was observed using transmission electron microscopy (TEM). Reactive oxygen species in bacterial cells were measured using flow cytometry with DCFH-DA staining. Results. Significant growth inhibition rate of E. coli cells was observed after photodynamic action of hypocrellin B. Remarkable damage to the ultrastructure of E. coli was also observed by TEM. Flow cytometry and CLSM observation showed that light-activated hypocrellin B markedly increased membrane permeability of E. coli. Flow cytometry showed the intracellular ROS increase in E. coli treated by photodynamic action of hypocrellin B. Conclusion. Light-activated hypocrellin B caused intracellular ROS increase and structural damages and inhibited the growth of Gram-negative E. coli cells.

The article focuses on a research on mucosal immunity enhanced by dietary Apostichopus japonicus. Topics discussed include role of lysozyme as innate immune effector located at mucosal surfaces to prevent infections, immunomodulatory efficacy of sea cucumbers and, better effects of A. japonicus ameliorated lysozyme on respiratory organs of immunosuppressive mice.