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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

BackgroundThe pathogenesis of post-stroke depression (PSD) remains largely unknown. There is growing evidence indicating that gut microbiota participates in the development of brain diseases through the gut-brain axis. Here, we aim to determine whether and how microbial composition and function altered among control, stroke and PSD rats.Materials and MethodsAfter the PSD rat model was successfully established, gut microbiome combined with fecal metabolome approach were performed to identify potentially PSD-related gut microbes and their functional metabolites. Then, correlations between behavior indices and altered gut microbes, as well as correlations between altered gut microbial operational taxonomic units (OTUs) with differential metabolites in PSD rats were explored. Enrichment analysis was also conducted to uncover the crucial metabolic pathways related to PSD.ResultsAlthough there were some alterations in the microbiome and metabolism of the control and stroke rats, we found that the microbial and metabolic phenotypes of PSD rats were significantly different. The microbial composition of PSD showed a decreased species richness indices, characterized by 22 depleted OTUs mainly belonging to phylum Firmicutes, genus Blautia and Streptococcus. In addition, PSD was associated with disturbances of fecal metabolomics, among them Glutamate, Maleic acid, 5-Methyluridine, Gallocatechin, 1,5-Anhydroglucitol, L-Kynurenine, Daidzein, Cyanoalanine, Acetyl Alanine and 5-Methoxytryptamine were significantly related to disturbed gut microbiome (P ≤ 0.01). Disordered fecal metabolomics in PSD rats mainly assigned to lipid, amino acid, carbohydrate and nucleotide metabolism. The steroid biosynthesis was particularly enriched in PSD.ConclusionsOur findings suggest that gut microbiome may participate in the development of PSD, the mechanism may be related to the regulation of lipid metabolism.

In recent years, with the deepening understanding of the gut microbiota, it has been recognized to play a significant role in the development and progression of diseases. Particularly in gastrointestinal tumors, the gut microbiota influences tumor growth by dysbiosis, release of bacterial toxins, and modulation of host signaling pathways and immune status. Immune checkpoint inhibitors (ICIs) have greatly improved cancer treatment efficacy by enhancing immune cell responses. Current clinical and preclinical studies have demonstrated that the gut microbiota and its metabolites can enhance the effectiveness of immunotherapy. Furthermore, certain gut microbiota can serve as biomarkers for predicting immunotherapy responses. Interventions targeting the gut microbiota for the treatment of gastrointestinal diseases, especially colorectal cancer (CRC), include fecal microbiota transplantation, probiotics, prebiotics, engineered bacteria, and dietary interventions. These approaches not only improve the efficacy of ICIs but also hold promise for enhancing immunotherapy outcomes. In this review, we primarily discuss the role of the gut microbiota and its metabolites in tumors, host immunity, and immunotherapy. [ABSTRACT FROM AUTHOR]

Background: In recent years, observational studies have provided evidence supporting a potential association between autism spectrum disorder (ASD) and gut microbiota. However, the causal effect of gut microbiota on ASD remains unknown. Methods: We identified the summary statistics of 206 gut microbiota from the MiBioGen study, and ASD data were obtained from the latest Psychiatric Genomics Consortium Genome-Wide Association Study (GWAS). We then performed Mendelian randomization (MR) to determine a causal relationship between the gut microbiota and ASD using the inverse variance weighted (IVW) method, simple mode, MR-Egger, weighted median, and weighted model. Furthermore, we used Cochran's Q test, MR-Egger intercept test, Mendelian Randomization Pleiotropy RESidual Sum and Outlier (MR-PRESSO), and leaveone- out analysis to identify heterogeneity and pleiotropy. Moreover, the Benjamin-Hochberg approach (FDR) was employed to assess the strength of the connection between exposure and outcome. We performed reverse MR analysis on the gut microbiota that were found to be causally associated with ASD in the forward MR analysis to examine the causal relationships. The enrichment analyses were used to analyze the biological function at last. Results: Based on the results of IVW results, genetically predicted family Prevotellaceae and genus Turicibacter had a possible positive association with ASD (IVW OR=1.14, 95% CI: 1.00-1.29, P=3.7x10-2), four gut microbiota with a potential protective effect on ASD: genus Dorea (OR=0.81, 95% CI: 0.69-0.96, P=1.4x10-2), genus Ruminiclostridium5 (OR=0.81, 95% CI: 0.69-0.96, P=1.5x10-2), genus Ruminococcus1 (OR=0.83, 95% CI: 0.70-0.98, P=2.8x10-2), and genus Sutterella (OR=0.82, 95% CI: 0.68-0.99, P=3.6x10-2). After FDR multiple-testing correction we further observed that there were two gut microbiota still have significant relationship with ASD: family Prevotellaceae (IVW OR=1.24; 95% CI: 1.09-1.40, P=9.2x10-4) was strongly positively correlated with ASD and genus RuminococcaceaeUCG005 (IVW OR=0.78, 95% CI: 0.67- 0.89, P=6.9x10-4) was strongly negatively correlated with ASD. The sensitivity analysis excluded the influence of heterogeneity and horizontal pleiotropy. Conclusion: Our findings reveal a causal association between several gut microbiomes and ASD. These results deepen our comprehension of the role of gut microbiota in ASD's pathology, providing the foothold for novel ideas and theoretical frameworks to prevent and treat this patient population in the future. [ABSTRACT FROM AUTHOR]

Background. The motor symptoms in patients with Parkinson's disease (PD) are commonly preceded by gastrointestinal (GI) symptoms. The enteric nervous system (ENS) has also been reported to exhibit neuropathological characteristics of PD. Objectives. To evaluate the relationship between the incidence of parkinsonism and alteration in gut microbiota and pathogens. Materials and methods. Studies in different languages that evaluate the relationship between gut microorganisms and PD were included into this meta-analysis. The outcomes of these studies were analyzed using a random effects model; it was also used to calculate the mean difference (MD) with 95% confidence interval (95% CI) in order to quantify the impact of different rehabilitation techniques on clinical parameters. Dichotomous and continuous models were used for the analysis of extracted data. Results. A total of 28 studies were included in our analysis. The analysis of small intestinal bacterial overgrowth showed a significant correlation with Parkinson's subjects compared with controls (p < 0.001). In addition, the presence of Helicobacter pylori (HP) infection was significantly related to the Parkinson's group (p < 0.001). On the other hand, there was a significantly higher abundance level of Bifidobacteriaceae (p = 0.008), Verrucomicrobiaceae (p < 0.001) and Christensenellaceae (p = 0.003) in Parkinson's subjects. In contrast, a significantly lower abundance levels in Parkinson's subjects were found in Faecalibacterium (p = 0.03), Lachnospiraceae (p = 0.005) and Prevotellaceae (p = 0.005). No significant difference was related to Ruminococcaceae. Conclusion. Parkinson's subjects showed a higher degree of alteration of gut microbiota and pathogens compared with normal human subjects. Future multicenter randomized trials are needed. [ABSTRACT FROM AUTHOR]

Background: Metabolic dysfunction-associated fatty liver disease (MAFLD) has become the most common chronic liver disease. MAFLD is a major risk factor for end-stage liver disease including cirrhosis and primary liver cancer. The pathogenesis of MAFLD is complex and has not yet been clarified. To the best of our knowledge, few studies have conducted quantitative bibliometric analysis to evaluate published MAFLD research. In this study, we conducted a comprehensive analysis of MAFLD publications over the past decade to summarize the current research hotspots and predict future research directions in this field. Methods: Articles into MAFLD published from 2012 to 2021 were identified from the Science Citation Index-Expanded of Web of Science Core Collection. CiteSpace software, VOSviewer, the "bibliometrix" R package, and the Online Analysis Platform of Literature Metrology were used to analyze the current publication trends and hotspots. Results: We retrieved 13959 English articles about MAFLD published from 2012 to 2021. Primary sites of publication were dominated by the United States until 2014, when China became the source of most published MAFLD-related research papers. The United States was found to be the most engaged country in international cooperative efforts. Shanghai Jiao Tong University was the most productive institution. Loomba R was the most productive author with 123 articles. The co-cited keyword cluster tag showed ten main clusters: #0 liver fibrosis, #1 hemoglobin, #2 metabolic associated fatty liver disease, #3 egcg, #4 myocardial infarction, #5 heart disease, #6 pnpla3, #7 hepatocellular carcinoma, #8 noninvasive marker, and #9 children. Keyword burst analysis showed that gut microbiota was the highest-intensity research hotspot. Conclusion: In the past decade, the number of publications on MAFLD increased dramatically, especially in the last three years. Gut microbiota became an important research direction for etiological and therapeutic investigations into MAFLD. Insulin resistance was also a key factor in studying the development of MAFLD in recent years. Liver fibrosis was an important focus of disease development. This study provides systematic information, helps guide future research, and helps to identify mechanisms and new treatment methods for MAFLD. [ABSTRACT FROM AUTHOR]

Background. Diet, environment, and genomic context have a significant impact on humans' intestinal microbiota. Moreover, migration may be accompanied by changes in human eating habits and living environment, which could, in turn, affect the intestinal microbiota. Located in southwestern China, Tibet has an average altitude of 4,000 meters and is known as the world's roof. Xianyang is situated in the plains of central China, with an average altitude of about 400 meters. Methods. To understand the association between intestinal microbiota and population migration, we collected the fecal samples from 30 Tibetan women on the first day (as TI1st), six months (as TI2nd), and ten months (as TI3rd) following migration from Tibet to Xianyang. Fecal samples were collected from 29 individuals (belonging to the Han women) as a control. The dietary information of the Tibetan women and the Han women was gathered. We performed a 16S rRNA gene survey of the collected fecal samples using Illumina MiSeq sequencing. Results. Following the migration, the alpha and beta diversity of Tibetan women's intestinal microbiota appeared unaffected. Linear discriminant analysis effect size (LEfSe) analysis showed that Klebsiella, Blautia, and Veillonella are potential biomarkers at TI1st, while Proteobacteria and Enterobacteriaceae were common in TI3rd. Finally, functional prediction by phylogenetic investigation of communities by reconstruction of unobserved states (PICRUSt) found no significant up-regulation or down-regulation gene pathway in the intestinal microbiota of Tibetan women after migration. The present study reveals that the higher stability in Tibetan women's intestinal microbiota was less affected by the environment and diet, indicating that Tibetan women's intestinal microbiota is relatively stable. The main limitations of the study were the small sample size and all volunteers were women. [ABSTRACT FROM AUTHOR]

Accumulating evidence has suggested the importance of gut microbiota in the development of type 2 diabetes mellitus (T2DM). In the present study, 40 patients with T2DM were treated with liraglutide for 4 months. Feces samples and clinical characteristics were collected from these 40 T2DM patients before and after the liraglutide treatment. The diversity and composition of gut microbiota in the two groups were determined by sequencing the V4 region of bacterial 16S rRNA genes. Meanwhile, blood glucose, insulin, hemoglobin A1c (HbA1c), and lipid metabolism were also measured in the pre- and post-liraglutide-treatment groups. Wefind that Baseline HbA1c was associated with liraglutide treatment response (R2 D0:527, β = -0:726, p<0:0001). After adjusted for baseline HbA1c, blood urea nitrogen was associated with liraglutide treatment response. Besides, our results showed reduced gut microbial alpha diversity, different community structure distribution and altered microbial interaction network in patients treated with liraglutide. The liner discriminant analysis (LDA) effect size (LEfSe) analysis showed that 21 species of bacteria were abundant in the pre-liraglutide-treatment group and 15 species were abundant in the post-liraglutide-treatment group. In addition, we also find that Megamonas were significantly correlated with older age, diabetes duration and diabetic retinopathy, Clostridum were significantly correlated with family history of diabetes and Oscillospira were significantly correlated with both diabetic retinopathy and diabetic peripheral neuropathy. Functional analysis based on Kyoto Encyclopedia of Genes and Genomes (KEGG) and cluster of orthologous groups (COG) annotations enriched three KEGG metabolic pathways and six functional COG categories in the post-liraglutide-treatment group. In conclusion, our research suggests that baseline HbA1c, blood urea nitrogen and gut microbiota are associated with the liraglutide treatment applied on patients with T2DM. These findings may contribute to the beneficial effects of liraglutide against diabetes. [ABSTRACT FROM AUTHOR]

Campylobacter concisus was previously shown to be associated with inflammatory bowel disease including Crohn's disease (CD) and ulcerative colitis (UC). C. concisus has two genomospecies (GS). This study systematically examined the colonization of GS1 and GS2 C. concisus in the human gastrointestinal tract. GS1 and GS2 specific polymorphisms in 23S rRNA gene were identified by comparison of the 23S rRNA genes of 49 C. concisus strains. Two newly designed PCR methods, based on the polymorphisms of 23S rRNA gene, were developed and validated. These PCR methods were used to detect and quantify GS1 and GS2 C. concisus in 56 oral and enteric samples collected fromthe gastrointestinal tract of patients with IBD and healthy controls. Meta-analysis of the composition of the isolated GS1 and GS2 C. concisus strains in previous studies was also conducted. The quantitative PCR methods revealed that there was more GS2 than GS1 C. concisus in samples collected from the upper and lower gastrointestinal tract of both patients with IBD and healthy controls, showing that GS2 C. concisus is better adapted to the human gastrointestinal tract. Analysis of GS1 and GS2 composition of isolated C. concisus strains in previous studies showed similar findings except that in healthy individuals a significantly lower GS2 than GS1 C. concisus strains were isolated from fecal samples, suggesting a potential difference in the C. concisus strains or the enteric environment between patients with gastrointestinal diseases and healthy controls. This study provides novel information regarding the adaptation of different genomospecies of C. concisus in the human gastrointestinal tract. [ABSTRACT FROM AUTHOR]

Gastrointestinal probiotics are important members of intestinal microflora in both healthy animals and human beings, and these bacteria may reduce the risk of infection caused by certain opportunistic pathogens through exclusive inhibition, competition, and displacement. The lp_1643 protein on the cell surface of Lactobacillus plantarum WCFSI was assumed to possess a mucus-binding capability. This study aimed to determine if purified His-N2 protein exclusively inhibits pathogen adhesion to porcine mucus. The interaction of the His-N2 protein with porcine mucus was determined by indirect enzyme-linked immunosorbent assay (ELISA), and the adhesion was assessed by a traditional plating method to count the bacteria adhered to the porcine mucus. Indirect ELISA showed that His-N2 protein adhered to porcine mucus, and its interacting molecules existed. The His-N2 protein effectively inhibited the adhesion of Escherichia coli DH5α, Listeria monocytogenes CMCC54004, Salmonella Typhimurium ATCC 14028, and Shigella flexneri CMCC(B)51572 to porcine mucus. Results showed that inhibition of pathogen adhesion to porcine mucus depended on dose and strain. The adhesion of L. monocytogenes CMCC54004, Salmonella Typhimurium ATCC 14028, and S. flexneri CMCC(B)51572 was reduced by 95.7, 97.0, and 95.7%, respectively, by pre-adding 100 µl of 3.92 mg/ml of His-N2 protein, whereas that of E. coli DH5α was only 50.4%. The inhibition of adhesion of some pathogens by His-N2 was different at pH 6.6 and 7.5. The inhibition of E. coli DH5α, L. monocytogenes CMCC54004, and Salmonella Typhimurium ATCC 14028 at pH 6.6 was significantly higher than that at pH 7.5, whereas no statistically significant difference was observed in S. flexneri CMCC(B)51572. These results suggest that various types of inhibition mechanisms of His-N2 were involved in different pathogens. [ABSTRACT FROM AUTHOR]

To investigate the effects of luteolin (LUT) on the growth, antioxidant capacity, non−specific immunity and intestinal microbiota of red swamp crayfish (Procambarus clarkii), 300 individual crayfish (4.17 ± 0.50 g average body weight and 50.19 ± 1.40 mm average body length) were randomly divided into five groups and fed with LUT doses of 0 mg/kg (CG), 50 mg/kg (LG50), 100 mg/kg (LG100), 300 mg/kg (LG300), and 500 mg/kg (LG500) for 8 weeks, respectively. Firstly, the results demonstrated that the survival and growth performance were significantly improved in all LUT added groups compared to the control (CG group), with no significant differences in hepatosomatic index, feed coefficient and muscle components, and the crayfish in LG100 group showed the maximal survival rate (SR) and specific growth rate (SGR) (P < 0.05). Secondly, histological observations displayed that the hepatopancreas and intestine tissues were not impacted in the LUT−supplemented groups, and the length of intestinal folds was significantly increased in LG100 and LG300 groups. Thirdly, LG50, LG100, and LG300 groups produced significantly increased hepatopancreatic antioxidant enzyme activities and hemolymph immune indicators compared with the control. In all experimental groups, malondialdehyde (MDA) contents were significantly reduced, as were aspartate aminotransferase and alanine aminotransferase activities. Lastly, dietary LUT specifically improved the structure and optimized the function of the gut microbiota. Compared to the control, the LG100 group displayed a significant increase in the index of Chao1 and Observed species, an increase in the relative abundance of Proteobacteria and Actinobacteria, a decrease in the ratio of Bacteroidetes to Firmicutes, and an increase in the abundance of Thermomonas , Turicibacter , Bdellovibrio and Enterococcus. PICRUSt analysis demonstrated a significant improvement in the KEGG pathway associated with isoflavone biosynthesis in the LG group. In conclusion, the present study confirms that dietary supplementation with 50−300 mg/kg LUT favors growth, non−specific immunity and antioxidant function in P. clarkii , with optimal additions ranging from 102−165 mg/kg. Furthermore, it optimized gut microbiota function, suggesting that LUT can be used as a potential feed additive for P. clarkii. These findings provide new insights for crayfish's healthy culture. • The optimal level of LUT addition to P. clarkii diet was 102−165 mg/kg. • Dietary addition of LUT improved the survival and growth performance of P. clarkii. • Dietary addition of LUT enhanced the antioxidant and immune capacity of P. clarkii. • Dietary addition of LUT improved intestinal microbiota structure of P. clarkii. [ABSTRACT FROM AUTHOR]

The red swamp crayfish (Procambarus clarkii) is an important farming species in China and there is a high degree of overlap between the main crayfish production areas and areas contaminated with the heavy metal lead (Pb), thus putting crayfish farming at potential risk of Pb contamination. To assess the toxic effects of Pb on crayfish, in this study they were exposed to different concentrations of Pb (0, 0.1, 1, 10, 50 mg/L) for 72 h, and 0.1 mg/L represents the level of Pb in the contaminated water. Histomorphology and activities of antioxidant or immune-related enzymes suggest that the damage of Pb to the hepatopancreas and intestine was dose- and time-dependent, with the intestine being more sensitive to Pb than the hepatopancreas. Notably, after a short period (24 h) of stress at low concentrations (0.1 mg/L) of Pb, the malondialdehyde (MDA) content and antioxidant enzymes such as catalase (CAT) and glutathione peroxidase (GSH-Px) in the intestine of crayfish showed significant changes, indicating that low concentrations of Pb were also highly detrimental to crayfish. High-throughput sequencing of the intestinal microbial community indicated that Pb exposure led to a disturbance in the relative abundance of intestinal bacteria, increasing the abundance of pathogenic bacteria (Bosea, Cloacibacterium, Legionella spp.) and decreasing the abundance of potentially beneficial bacteria (Chitinibacter, Chitinilyticum, Paracoccus, Microbacterium, Demequina , and Acinetobacter spp.). In conclusion, Pb damages the hepatopancreas and intestinal barrier of crayfish, leading to the destruction of their anti-stress ability and immune response, and at the same time disrupts the homeostasis of intestinal microbes, resulting in adverse effects on the gut. This study contributed to the assessment of the ecotoxicity of the heavy metal Pb to the crustacean aquatic animals. [ABSTRACT FROM AUTHOR]