Analysis Of Intestinal Microbiota Research Articles

Omics Analyses of Intestinal Microbiota and Hypothalamus Clock Genes in Circadian Disturbance Model Mice Fed with Green Tea Polyphenols.

Green tea polyphenols (GTP) have similar activities as prebiotics, which effectively regulate the structure of intestinal flora and affect their metabolic pathways. The intestinal flora is closely related to the host's circadian rhythm, and the supplementation with GTP may be an effective way to improve circadian rhythm disorders. In this study, we established a mouse model of circadian rhythm disturbance of anthropogenic flora to investigate the regulation mechanism of GTP on the host circadian rhythms. After 4 weeks of GTP administration, the results showed that GTP significantly alleviated the structural disorder of intestinal microbiota, thus effectively regulating related metabolites associated with brain nerves and circadian rhythms. Moreover, single-cell transcription of the mouse hypothalamus suggested that GTP up-regulated the number of astrocytes and oligodendrocytes and adjusted the expression of core clock genes Csnk1d, Clock, Per3, Cry2, and BhIhe41 caused by circadian disruption. Therefore, this study provided evidence that GTP can improve the physiological health of hosts with the circadian disorder by positively affecting intestinal flora and related metabolites and regulating circadian gene expression.

Alteration of gut microbiota composition and function of Indian major carp, rohu (Labeo rohita) infected with Argulus siamensis

Gut microbiome homeostasis is critical in preventing diseases. However, the effect of disease on gut microbiota assembly remains unclear. At present, there are no reports on the composition and functional analysis of intestinal microbiota of Indian major carp, rohu (L. rohita) infected with ectoparasite, Argulus. In this study, we analysed and compared the intestinal microbiota of healthy and Argulus-infected rohu by 16S rRNA amplicon sequencing. Argulus infection could significantly influence the diversity and richness of the gut microbiota. However, abundance of Actinobacteria and Patescibacteria were enriched significantly in Argulus-infected fish. Venn diagram revealed that there were many more unique genera in the infected group as compared to control fish. The genera, Stenotrophomonas and Pirellula were significantly increased in infected fish while the abundance of Reyranella was decreased. LEfSe analysis showed a significant enrichment in abundances of 11 taxa in healthy group and 17 taxa in infected group. Furthermore, genera Rubellimicrobium, Dielma, Hyphomicrobium, Reyranella, Streptomyces and Cloacibacterium performed the best in differentiating between both the groups. Predicted microbiota function by PICRUSt revealed that the gut microbiota of infected fish was mainly associated with enriched synthesis of chitinases, chitin binding proteins, osmoprotectant proteins and sulfatases enzymes. There was a positive association between the structural and functional composition of the gut microbiota. The results indicated that the Argulus infection could affect the intestinal microbiota composition and function of rohu.

Alterations in intestinal microbiota composition coincide with impaired intestinal morphology and dysfunctional ileal immune response in growing-finishing pigs under constant chronic heat stress

BackgroundPrevious studies had shown that short-term acute heat stress (HS) affected the host’s metabolism and intestinal microbiota independent of feed intake (FI) reduction, and long-term calorie restriction caused intestinal morphological injuries and gut microbial alterations. However, research on the effects of constant chronic HS on intestinal microbial composition and the roles of FI reduction played in is limited. This study aimed to investigate the effects of 7-day constant chronic HS on the composition of intestinal microbes in growing-finishing pigs, and its relationship with pigs’ performance, intestinal morphology, and ileal immune response. Twenty-four growing-finishing pigs (Duroc × Large White × Landrace, 30 ± 1 kg body weight) were randomly assigned to three treatments (n = 8), 1) thermal neutral (TN) conditions (25 ± 1 °C) with ad libitum FI, 2) HS conditions (35 ± 1 °C) with ad libitum FI, 3) pair-fed (PF) with HS under TN conditions to discriminate the confounding effects of dissimilar FI, and the FI was the previous day’s average FI of HS. The small intestinal segments (duodenum, jejunum, and ileum) and feces were collected on d 8.ResultsResults indicated that HS drastically declined (P < 0.05) average daily gain (ADG) and average daily feed intake (ADFI) (about 61%) in comparison with TN, and caused hyperpyrexia, meanwhile PF caused hypothermia. Morphological observation by light and electron microscopes showed that both HS and PF treatment decreased (P < 0.05) the villus and microvillus height compared with TN. Additionally, HS increased (P < 0.05) protein expression of heat shock protein 70 in the duodenum, jejunum, and ileum. Furthermore, the expression of tight junction protein zonula occluden-1 (ZO-1) in the duodenum and ileum, and Occludin in the ileum were enhanced (P < 0.05) compared with TN and PF. Moreover, HS significantly enhanced (P < 0.05) the mRNA relative expression of inflammatory cytokines (TLR-2, TLR-4, and tumor necrosis factor-α (TNF-α), IL-6, IL-8, PG1–5, β-defensin 2 (pBD-2)), mucins (mucin-1 and mucin-2) and P65 protein level in the ileal mucosa tissue. Intestinal microbiota analysis by 16S rRNA sequencing showed lower (P < 0.10) α diversity in both HS and PF, and a separated cluster of β diversity among groups. Compared with TN, HS but not PF mainly reduced (FDR < 0.05) Bacteroidetes (phylum), Bacteroidia (class) and elevated the proportions of Proteobacteria (phylum, FDR < 0.05), Bacillales (order, FDR < 0.05), Planococcaceae (family, FDR < 0.05), Kurthia (genus, FDR < 0.05), Streptococcaceae (family, FDR < 0.10) and Streptococcus (genus, FDR < 0.10). Notably, Lactobacillales (order) was decreased (FDR < 0.05) by PF alone. Furthermore, the Spearman correlation analysis indicated that the microbes prevalent in HS were positively (P < 0.05) associated with intestinal morphological injuries indicators and ileal immune response parameters, and the microbes reduced in HS were negatively (P < 0.05) with the performance data.ConclusionsIntestinal morphological injuries and ileal immune response caused by constant chronic HS independent of FI showed close connections with alterations in intestinal microbiota in growing-finishing pigs.

Hydroxyapatite-coated titanium oxide ameliorates dextran sulphate sodium-induced colitis by attenuating both innate and acquired immune reaction.

Titanium oxide (TiO2) is a widely used oxidizer for environmental management. The power of TiO2 has been demonstrated by its photocatalytic activity. Hydroxyapatite (HA)-coated TiO2 (HA-TiO2) was used to test the in vivo effect on dextran sulphate sodium (DSS)-induced colitis in mice. Mice were monitored for body weight and then sacrificed on the seventh day, and the colon length was measured. Their faeces were analysed for intestinal microbiota distribution, and colon tissue was subjected to histological examination and immunohistochemical analysis. Weight loss was significantly lower in HA-TiO2-fed mice than in mice without HA-TiO2. The colon length in the DSS colitis-induced mice was shortened, but HA-TiO2 feeding lessened this effect. Histological and immunohistochemical analyses of the colon revealed that macrophages and CD4+CD8+ T cells were observed in the colitis-occurring site, indicating the involvement of innate and acquired immunity in determining the degree of DSS-induced colitis. Intestinal microbiota analysis in faeces revealed changes in the distribution of multiple bacterial species after DSS colitis induction, and the increase/decrease of 2 Clostridium (sub)clusters moved in response to the colitis phenomenon. All the described effects of HA-TiO2 were photocatalytic activity-dependent because mice that were kept in the dark showed similar results to those treated with DSS alone without HA-TiO2. HA-coated TiO2 ameliorated DSS-induced colitis through photocatalytic activity, while HA-TiO2 diminished the changes in intestinal microbiota and immune reactions caused by DSS.

Диагностическая роль определения кальпротектина у детей с муковисцидозом

Cystic fibrosis (CF) is characterized by chronic intestinal inflammation and small intestinal bacterial overgrowth. In recent years, the correlation between calprotectin and gastrointestinal manifestations (intestinal diseases, abdominal pain syndrome) in CF has been actively studied. Objective. To study the level of fecal calprotectin in children with CF and evaluate its clinical significance. Patients and methods. A total of 67 children with CF aged between 1 and 18 years (mean age 7 (±4.0) years) were examined using a cross-sectional study design. All children were divided into 3 groups according to calprotectin concentrations: group 1 – &lt;50 μg/g, group 2 – 50–120 μg/g, group 3 – &gt;120 μg/g. Clinical and anamnestic data, nutritional status, and microbiological diagnosis were analyzed; a microbiological analysis of the large intestinal microbiota was conducted to determine the nature of biocenosis disorders; a coprological analysis was performed; fecal calprotectin concentrations were evaluated. Conclusion. Calprotectin cannot serve as a marker of enterocolitis/enteropathy in CF, which is сconsistent with the findings of the ESPGHAN expert group. Calprotectin determination in children with CF without clinical manifestations of inflammatory bowel disease is not informative. Calprotectin does not refer to indicators that determine the presence of infectious enterocolitis, the severity of the course and the outcome of the disease. Key words: calprotectin, children, cystic fibrosis, microbiota, intestinal syndrome, clostridia

Protective mechanism of homologous lactic acid bacteria against cholestatic liver injury in snakehead fish

Cholestatic liver injury, a typical symptom of hepatobiliary syndrome, is usually accompanied by bile acid (BA) metabolism disorders and intestinal microbiota imbalance. Lactic acid bacteria (LAB) play an active role in regulating liver and gallbladder diseases and the balance of intestinal microbiota. In the study, the protective mechanism of homologous LAB (Lactococcus lactis L19, Genbank: MT102745.1) isolated from the intestine of snakehead fish (Channa argus, C. argus) against lithocholic acid (LCA)-induced cholestatic liver injury in C. argus was explored. Biochemical results illustrated that LCA feeding markedly increased the serum AST, ALT, ALP, TBA, TBIL and DBIL activities and treatment with L19 diet reversed the increase of these BA biomarkers. Liver histology results identified the amelioration of LCA-induced cholestasis after L19 treatment. Gene analysis indicated that L19 activated fxr and regulated BA metabolism, including promoted BA transport from the liver into the intestine by inducing the expressions of fxr-target genes bsep, mrp2, mrp3, mrp4, and Ostβ, and reduced BA reabsorption by inhibiting the expression of ntcp. In addition, L19 reduced BA synthesis by inhibiting the expressions of fxr-target genes cyp7a1, cyp8b1, cyp27a1, and hmgcr via the Fxr-Shp signaling pathway, and promoted BA metabolism by inducing the expression of sult2a1. Protein analysis indicated that L19 promoted BA metabolism and transport through activating the Fxr-target proteins Bsep, Shp and Cyp7a1. Intestinal microbiota analysis demonstrated that the LCA group was dominated by Proteobacteria and Chlamydiae, while L19 treatment can reduce the abundance of Proteobacteria, increase the abundance of Firmicutes, and regulate the composition of intestinal microbiota. For the first time, we found that L. lactis L19 can activate Fxr, regulate BA metabolism and intestinal microbiota to exert protective effects against cholestatic liver injury. Therefore, L. lactis L19 might be a potent measure for the prevention against LCA-induced cholestatic liver injury of fish, possibly via Fxr-Bsep and Fxr-Shp signal pathway and intestinal microbiota alteration.

Combined Intestinal Metabolomics and Microbiota Analysis for Acute Endometritis Induced by Lipopolysaccharide in Mice.

Endometritis is generally caused by bacterial infections, including both acute and chronic infections. In the past few decades, accumulated evidence showed that the occurrence of diseases might be related to gut microbiota. The progression of diseases is previously known to change the composition and diversity of intestinal microbiota. Additionally, it also causes corresponding changes in metabolites, primarily by affecting the physiological processes of microbiota. However, the effects of acute endometritis on intestinal microbiota and its metabolism remain unknown. Thus, the present study aimed to assess the effects of acute endometritis on intestinal microbes and their metabolites. Briefly, endometritis was induced in 30 specific pathogen-free (SPF) BALB/c female mice via intrauterine administration of lipopolysaccharide (LPS) after anesthesia. Following this, 16S rRNA gene sequencing and liquid chromatogram-mass spectrometry (LC-MS) were performed. At the genus level, the relative abundance of Klebsiella, Lachnoclostridium_5, and Citrobacter was found to be greater in the LPS group than in the control group. Importantly, the control group exhibited a higher ratio of Christensenellaceae_R−7_group and Parasutterella. Furthermore, intestinal metabolomics analysis in mice showed that acute endometritis altered the concentration of intestinal metabolites and affected biological oxidation, energy metabolism, and biosynthesis of primary bile acids. The correlation analysis between microbial diversity and metabolome provided a basis for a comprehensive understanding of the composition and function of the microbial community. Altogether, the findings of this study would be helpful in the prevention and treatment of acute endometritis in the future.

Comparative chronic toxicities of PFOS and its novel alternatives on the immune system associated with intestinal microbiota dysbiosis in adult zebrafish

6:2 Chlorinated polyfluorinated ether sulfonate (F-53B) and sodium p-perfluorous nonenoxybenzene sulfonate (OBS) are widely used as perfluorooctane sulfonate (PFOS) alternatives in the Chinese market. Here, adult zebrafish were chronically exposed to 1 μM PFOS, F-53B, and OBS for 21 days to investigate the comparative immunotoxicity of these three per- and polyfluoroalkyl substances (PFAS). PFOS induced more severe oxidative stress in the liver than F-53B and OBS, and these three PFAS induced similar anti-inflammatory effects by repressing the expression of pro-inflammatory cytokines. The intestinal microbiota analysis showed that the relative abundance of Plesiomonas, Aeromonas, Cetobacterium, Shewanella, and Vibrio changed with the same trend in the three PFAS treatment groups. Furthermore, the PFAS increased the expression of hepcidin, muc, the immune-related genes mpo and saa, and decreased the expression of the tight junction-related gene occ in the intestine; moreover, villus height of the intestine was reduced after PFAS exposure, which indicated the functional disruption of the intestine. In particular, the significant correlation between the changed intestinal microbiota and liver and intestinal indicators also suggested the interaction between the immune system and intestinal microbiota. Taken together, our results indicate that exposure to PFOS and its alternatives F-53B and OBS can induce hepatic immunotoxicity associated with intestinal microbiota dysbiosis in adult zebrafish.

Intestinal dysbiosis promotes immune dysregulation in an animal model of Alzheimer's disease.

Current evidence suggests that systemic inflammation promotes Alzheimer's Disease (AD) and recent reports demonstrated that circulating neutrophils migrate into the AD brain inducing neuroinflammation and cognitive deficits in animal models of AD. However, how peripheral immune dysregulation occurs and promotes neuroinflammation and memory decline in AD is still unknown. Even though descriptive reports suggest the involvement of the microbiome in AD, the mechanisms behind AD pathology are not explored. In this context, we aim to better understand the dysregulation of leukocyte subpopulations in AD by addressing the gut-blood-brain axis. By taking advantage of the 3xTg-AD mouse model we addressed peripheral inflammation during early disease stages. To this aim, we performed: 1) an intestinal microbiota analysis; 2) characterization of circulating inflammatory mediators; and 3) immunophenotypization of peripheral blood. In our study we show a clear intestinal dysbiosis in the 3xTg-AD mice, characterized by higher abundance of taxa known to cause proinflammatory conditions. In agreement, we also found increased intestinal permeability and accumulation of immature precursors and aged neutrophils in circulating blood, suggesting a strong peripheral dysregulation in the early phases of the disease. Altogether, our data suggest microbiota as a modulator of leukocyte activation and migration into the brain. Therefore, targeting the gut-blood-brain axis in AD could lead to new immunomodulatory strategies for AD treatment.

Influence of Light/Dark Cycles on Body Color, Hepatopancreas Metabolism, and Intestinal Microbiota Homeostasis in Litopenaeus vannamei

In aquatic animals, the light/dark cycle acts as an important biological factor that influences the entire life cycle. Until present, evidence regarding the regulation of physiological metabolic process under different light/dark cycles is limited in Litopenaeus vannamei. In this study, we mainly investigated the effects of different light/dark cycles (12 h light/12 h dark, 0 h light/24 h dark) on the hepatopancreas metabolism and intestinal microbiota homeostasis in L. vannamei using multiomics techniques. One interesting finding was that the body color of L. vannamei became darker after dark treatment for 8 weeks. Further hepatopancreas transcriptome analysis identified down-regulated genes involved in regulating nutrition metabolism, body-color formation, diurnal rhythm, immune function, hormone levels, and posttranslational modifications. The intestinal microbiota analysis showed that dark treatment-induced alterations in intestinal bacterial abundances in L. vannamei, such as decreased (P &amp;lt; 0.05) relative abundance of Formosa, Demequina, Lutimonas and increased (P &amp;lt; 0.05) relative abundance of Ruegeria, Vibrio, Actibacter, Roseovarius, Ilumatobacter, and Kriegella at the genus level. The microbiota functional analysis demonstrated that the dark treatment mainly increased susceptibility of pathogens, decreased nutrition metabolism, and influenced circadian rhythm. This study indicated for the first time that constant darkness treatment darkened the body color and altered hepatopancreas metabolism and intestinal microbiota homeostasis in L. vannamei, which might give potential clues for improving the productive capacities by changing light/dark cycles in shrimp farming.

Alteration of the gut microbiota in rhesus monkey with spontaneous osteoarthritis

BackgroundThe spontaneous osteoarthritis (OA) in rhesus macaque is similar to OA in human, which maintains an upright body posture and shows very similar biomechanical properties of bones to humans. At present, there is no good treatment for OA. This study aims to explore relationship between OA and intestinal microbiota, and provide a reference for the treatment of clinical OA.ResultsWe collected colonic contents of the 20 rhesus macaque (6–15 years old, female) for intestinal microbiota analysis by metagenomics sequencing, of which 10 were spontaneous OA monkeys and 10 were normal monkeys. Our results showed the diversity of gut microbiota in monkeys with OA was decreased compared to the normal monkeys (p = 0.16). Mollicutes, Tenericutes, Coprobacillus and Faecalitalea may be biomarkers for the monkeys of OA. Lactobacillus found significantly increased in OA monkeys. Prevotella and Ruminococcus were higher in the normal group than OA group. Zinc/manganese transport system permease protein (p = 0.0011) and Cyclopropane-fatty-acyl-phospholipid synthase (p = 0.0012) are a microbiota metabolic pathway related to cartilage production.ConclusionsOur results indicate that the diversity and composition of intestinal microbiota in monkeys with OA are different compared to the normal monkeys. we have found microbes that may be a biomarker for the diagnosis of osteoarthritis. Functional analysis of the microbiota also predicts cartilage damage in the monkeys with osteoarthritis. Non-human primates are closely related to humans, so this study can provide a reference for the development of drugs for the treatment of OA.

Pediococcus pentosaceus Enhances Host Resistance Against Pathogen by Increasing IL-1β Production: Understanding Probiotic Effectiveness and Administration Duration.

Probiotic administration is a potential strategy against enteric pathogen infection in either clinical treatment or animal nutrition industry, but the administration duration of probiotics varied and the underlying mechanisms remain unclear. A strain (YC) affiliated to Pediococcus pentosaceus, a commonly used probiotic, was isolated from fish gut and the potential role of YC against Aeromonas hydrophila was detected in zebrafish. We found that 3- or 4-week YC administration (YC3W or YC4W) increased the resistance against A. hydrophila while 1- or 2-week treatment (YC1W or YC2W) did not. To determine the possible reason, intestinal microbiota analysis and RNAseq were conducted. The results showed that compared with CON and YC1W, YC4W significantly increased the abundance of short-chain fatty acids (SCFAs) producing bacteria and elevated the gene expression of nlrp3. Higher butyrate content and enhanced expression of IL1β were subsequently found in YC4W. To identify the causal relationship between butyrate and the higher pathogen resistance, different concentrations of sodium butyrate (SB) were supplemented. The results suggested that 10 mmol/kg SB addition mirrored the protective effect of YC4W by increasing the production of IL-1β. Furthermore, the increased IL-1β raised the percentage of intestinal neutrophils, which endued the zebrafish with A. hydrophila resistance. In vivo knockdown of intestinal il1b eliminated the anti-infection effect. Collectively, our data suggested that the molecular mechanism of probiotics determined the administration duration, which is vital for the efficiency of probiotics. Promoting host inflammation by probiotic pretreatment is one potential way for probiotics to provide their protective effects against pathogens.

The Role of Fecal Fusobacterium nucleatum and pks+ Escherichia coli as Early Diagnostic Markers of Colorectal Cancer.

Background Accurate analysis of intestinal microbiota will facilitate establishment of an evaluating system for assessing colorectal cancer (CRC) risk and prognosis. This study evaluates the potential role of Fusobacterium nucleatum (F. nucleatum) and Escherichia coli with a pks gene (pks+ E. coli) in early CRC diagnosis. Methods We recruited 139 patients, including CRC (n = 60), colorectal adenomatous polyposis (CAP) (n = 37), and healthy individuals (n = 42) based on their colonoscopy examinations. We collected stool and serum samples from the participants and measured the relative abundance of F. nucleatum and pks+ E. coli in fecal samples by quantitative PCR. Receiver operating characteristic curve (ROC) analyses were used to analyze the diagnostic value of single or combined biomarkers. Results Fecal F. nucleatum and pks+ E. coli levels were higher in the CRC group in either the CAP group or healthy controls (P = 0.02; 0.01). There was no statistical difference in the distribution of F. nucleatum and pks+ E. coli in patients with different tumor sites (P > 0.05). The combination of F. nucleatum+pks+ E. coli+CEA+CA19-9+FOBT was chosen as the optimal panel in differentiating both CRC and CAP from the controls. The combination of F. nucleatum, pks+ E. coli, and FOBT improved diagnostic efficiency. However, there was difficulty in differentiating CRC from CAP. Conclusion Our results suggested that combining bacterial markers with conventional tumor markers improves the diagnostic efficiency for noninvasive diagnosis of CRC.

Role of TLR5 in the Translocation and Dissemination of Commensal Bacteria in the Intestine after Traumatic Hemorrhagic Shock.

Enterogenous infection is a major cause of death during traumatic hemorrhagic shock (THS). It has been reported that Toll-like receptor 5 (TLR5) plays an integral role in regulating mucosal immunity and intestinal homeostasis of the microbiota. However, the roles played by TLR5 on intestinal barrier maintenance and commensal bacterial translocation post-THS are poorly understood. In this research, we established THS models in wild-type (WT) and Tlr5−/− (genetically deficient in TLR5 expression) mice. We found that THS promoted bacterial translocation, while TLR5 deficiency played a protective role in preventing commensal bacteria dissemination after THS. Furthermore, intestinal microbiota analysis uncovered that TLR5 deficiency enhanced the mucosal biological barrier by decreasing RegIIIγ-mediated bactericidal activity against G+ anaerobic bacteria. We then sorted small intestinal TLR5+ lamina propria dendritic cells (LPDCs) and analyzed TH1 differentiation in the intestinal lamina propria and a coculture system consisting of LPDCs and naïve T cells. Although TLR5 deficiency attenuated the regulation of TH1 polarization by LPDCs, it conferred stability to the cells during THS. Moreover, retinoic acid (RA) released from TLR5+ LPDCs could play a key role in modulating TH1 polarization. We also found that gavage administration of RA alleviated bacterial translocation in THS-treated WT mice. In summary, we documented that TLR5 signaling plays a pivotal role in regulating RegIIIγ-induced killing of G+ anaerobic bacteria, and LPDCs mediated TH1 differentiation via RA. These processes prevent intestinal bacterial translocation and enterogenous infection after THS, suggesting that therapeutically targeting LPDCs or gut microbiota can interfere with bacterial translocation after THS.

Multi-Omics Analysis to Generate Hypotheses for Mild Health Problems in Monkeys.

Certain symptoms associated with mild sickness and lethargy have not been categorized as definitive diseases. Confirming such symptoms in captive monkeys (Macaca fascicularis, known as cynomolgus monkeys) can be difficult; however, it is possible to observe and analyze their feces. In this study, we investigated the relationship between stool state and various omics data by considering objective and quantitative values of stool water content as a phenotype for analysis. By examining the food intake of the monkeys and assessing their stool, urine, and plasma, we attempted to obtain a comprehensive understanding of the health status of individual monkeys and correlate it with the stool condition. Our metabolomics data strongly suggested that many lipid-related metabolites were correlated with the stool water content. The lipidomic analysis revealed the involvement of saturated and oxidized fatty acids, metallomics revealed the contribution of selenium (a bio-essential trace element), and intestinal microbiota analysis revealed the association of several bacterial species with the stool water content. Based on our results, we hypothesize that the redox imbalance causes minor health problems. However, it is not possible to make a definite conclusion using multi-omics alone, and other hypotheses could be proposed.

Effects of moderate exercise on hepatic amino acid and fatty acid composition, liver transcriptome, and intestinal microbiota in channel catfish (Ictalurus punctatus)

Previous research on swimming exercise in fish has focused on muscle building and quality of flesh. However, the effects of hepatic amino acid and fatty acid composition, liver gene expression profile, and intestinal microbiota are poorly understood. In this study, channel catfish (Ictalurus punctatus) were subjected to a 4-week swimming exercise, and liver transcriptome and intestinal microbiota analyses were performed to broaden our understanding of fish under exercise. When compared to non-exercised channel catfish (N-EXF), exercised channel catfish (EXF) had improved arachidonic acid (C20:4n6; ARA), docosahexaenoic acid (C22:6n3; DHA), aspartic acid (Asp) and glycine (Gly). The liver transcriptome analysis revealed 2912 differentially expressed genes and numerous enriched signaling pathways including those involved in nutrient synthesis, such as biosynthesis of unsaturated fatty acids and amino acids; glucose metabolism, such as glycolysis/gluconeogenesis, insulin signaling, and AMPK signaling pathways; and oxygen transport, such as HIF-1, PI3K-Akt, and MAPK signaling pathways. In addition, bacterial 16S rRNA gene sequencing data revealed that long-term exercise increased bacterial diversity and richness, and changed the intestinal microbial composition in channel catfish. In summary, this study provides insights into hepatic metabolic pathways, candidate genes, and intestinal microbiota underlying the long-term exercised channel catfish.

Effects of dietary manganese supplementation on growth performance, antioxidant capacity, immune function and intestinal microbiota in Pacific white shrimp Litopenaeus vannamei

Water manganese (Mn) is apparently insufficient to meet aquatic animals’ metabolic requirement, and their food is considered as the major Mn source. Currently, researches reporting the effects of dietary Mn inclusion on physiological and metabolic function in Litopenaeus vannamei (L. vannamei) are very scarce. Therefore, 8-week feeding trail was conducted to determine dietary Mn requirement for L. vannamei and further evaluate the effects of dietary Mn supplementation on tissue Mn concentration, antioxidant enzyme activity, nonspecific immune enzymes activity and intestinal microbiota composition. Our results demonstrated that the optimum dietary Mn requirement for L. vannamei was determined to be 44.83 mg/kg based on the per cent weight gain; supplementing 39.57 mg/kg, 54.57 mg/kg and 72.67 mg/kg Mn significantly increased (p < .05) the activity of serum lysozyme (LZM), nitric oxide synthase and alkaline phosphatase, the activity of antioxidative capacity and glutathione in serum and hepatopancreas of L. vannamei. Supplementing 111.97 mg/kg Mn significantly increased (p < .05) hepatopancreas Mn concentration and serum LZM activity. Intestinal microbiota analysis showed that supplementing 39.57 mg/kg and 111.97 mg/kg Mn significantly influenced (p < .05) intestinal microbiota composition and function. These findings might help provide a scientific basis for the commercial application of Mn in L. vannamei.

Effects of Different Treatment Methods of Dried Citrus Peel (Chenpi) on Intestinal Microflora and Short-Chain Fatty Acids in Healthy Mice

Chenpi is a kind of dried citrus peel from Citrus reticulata, and it is often used as traditional Chinese medicine to treat dyspepsia and respiratory tract inflammation. In this study, to determine which way of chenpi treatment plays a better effect on the prevention of obesity in healthy mice, we conducted 16S ribosomal RNA (rRNA) gene sequencing for intestinal microbiota and gas chromatography-mass spectrometry detector (GC/MSD) analysis for short-chain fatty acids (SCFAs) of female rats fed with either chenpi decoction or chenpi powder-based diet (n = 10 per group) for 3 weeks. Chenpi powder (CP) group significantly reduced abdominal adipose tissues, subcutaneous adipose tissue, and the serum level of total triacylglycerol (TG). At a deeper level, chenpi powder has a better tendency to increase the ratio of Bacteroidetes to Firmicutes. It alters the Muribaculaceae and Muribaculum in intestinal microbiota, though it is not significant. The concentrations of acetic acid, valeric acid, and butyric acid increased slightly but not significantly in the CP group. Chenpi decoction just reduced perirenal adipose tissues, but it shows better antioxidant activity. It has little effect on intestinal microbiota. No differences were found for SCFAs in the chenpi decoction (CD) group. The results indicated that chenpi powder has a better effect in preventing obesity in mice. It can provide a basis for the development of functional products related to chenpi powder.

Effect of intestinal microbiota imbalance associated with chronic hepatitis B virus infection on the expression of microRNA‑192 and GLP‑1

It has been reported that hepatitis B virus (HBV) infection has an impact on intestinal microbiota imbalance to induce diabetes mellitus (DM), but the underlying mechanisms still remain to be explored. The present study aimed to investigate the regulatory role of microRNA‑192 (miR‑192‑5p) and glucagon‑like peptide‑1 (GLP‑1) in intestinal microbiota imbalance by recruiting patients with DM infected with HBV. In the present study, patients with HBV infection and different levels of alanine transaminase (ALT) were recruited and divided into three groups. Intestinal microbiota analysis was performed to evaluate the fecal bacterial composition of patients in various groups. Quantitative PCR was performed to explore the differential expression of miR‑192‑5p and GLP‑1 in the feces, peripheral blood and intestinal mucosal tissue samples of each patient. Immunohistochemistry was used to assess the expression of GLP‑1 protein in the intestinal mucosal tissue samples. Luciferase assays were performed by cell transfection of miR‑192‑5p mimics/precursors/inhibitors to study the inhibitory effect of miR‑192‑5p on GLP‑1 expression. Intestinal microbiota imbalance was observed in hepatitis B surface antigen (HBsAg)‑positive patients with high ALT. The expression of miR‑192‑5p was significantly elevated in the feces, peripheral blood and intestinal mucosal tissue samples of HBsAg‑positive patients with high ALT along with decreased GLP‑1 mRNA and protein expression. Luciferase activity of GLP‑1 vector was inhibited by miR‑192‑5p mimics and promoted by miR‑192‑5p inhibitors. Transfection of miR‑192‑5p precursors resulted in upregulation of miR‑192‑5p and downregulation of GLP‑1, while miR‑192‑5p inhibitors remarkably suppressed the expression of miR‑192‑5p and notably induced the expression of GLP‑1. These results showed a regulatory network involving HBV infection, intestinal microbiota imbalance, and miR‑192‑5p and GLP‑1 expression.

Stenotrophomonas strain CPCC 101271, an intestinal lifespan-prolonging bacterium for Caenorhabditis elegans that assists in host resistance to \u201cBacillus nematocida\u201d colonization

The soil-dwelling, opportunistic pathogenic bacterium "Bacillus nematocida" B16 exhibits strong killing activities against a variety of pathogenic nematodes via a “Trojan horse” mechanism that can kill worm species like Caenorhabditis elegans. The bacterial strain CPCC 101271 was previously isolated from the intestines of C. elegans that were recovered from natural habitats and can serve as a probiotic for C. elegans, while also assisting in resistance to infection by the pathogenic strain B16. In this study, the lifespan of C. elegans fed with strain CPCC 101271 cells was extended by approximately 40% compared with that of worms fed with Escherichia coli OP50 cells. In addition, the colonization of C. elegans by the pathogenic bacterium "B. nematocida" B16 was inhibited when pre-fed with strain CPCC 101271. Metagenomic sequence analysis of intestinal microbiota of C. elegans fed with strain CPCC 101271 and infected with B16 revealed that pre-feeding worms with CPCC 101271 improved the diversity of the intestinal bacteria. Moreover, community structure significantly varied in coordination with Stenotrophomonas spp. and Bacillus spp. abundances when competition between strains CPCC 101271 and B16 was evaluated. In conclusion, the nematode microbiota strain CPCC 101271 assisted in its host resistance to colonization by the pathogen "Bacillus nematocida" and can also promote life span-prolongation in C. elegans. These results underscore that understanding the interactions between C. elegans microbiota and pathogens can provide new insights into achieving effective biological control of agricultural pests.