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Frontiers in Sports and Active Living 2023The gut microbiome plays a fundamental role in host homeostasis through regulating immune functions, enzyme activity, and hormone secretion. Exercise is associated with...
INTRODUCTION
The gut microbiome plays a fundamental role in host homeostasis through regulating immune functions, enzyme activity, and hormone secretion. Exercise is associated with changes in gut microbiome composition and function. However, few studies have investigated the gut microbiome during training periodization. The present study aimed to investigate the relationship between training periodization and the gut microbiome in elite athletes.
METHODS
In total, 84 elite athletes participated in the cross-sectional study; and gut microbiome was determined during their transition or preparation season period. Further, 10 short-track speed skate athletes participated in the longitudinal study, which assessed the gut microbiome and physical fitness such as aerobic capacity and anaerobic power in the general and specific preparation phase of training periodization. The gut microbiome was analyzed using 16S rRNA sequencing.
RESULTS
The cross-sectional study revealed significant differences in and genera and in enterotype distribution between transition and preparation season phase periodization. In the longitudinal study, training phase periodization altered the level of , , and in the microbiome. Such changes in the microbiome were significantly correlated with alternations in aerobic capacity and tended to correlate with the anaerobic power.
DISCUSSION
These findings suggest that periodization alters the gut microbiome abundance related to energy metabolism and trainability of physical fitness. Athlete's condition may thus be mediated to some extent by the microbiota in the intestinal environment.
PubMed: 37521099
DOI: 10.3389/fspor.2023.1219345 -
Proceedings of the National Academy of... Aug 2022Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of pancreatic β-cells. One of the earliest aspects of this process is the development of...
Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of pancreatic β-cells. One of the earliest aspects of this process is the development of autoantibodies and T cells directed at an epitope in the B-chain of insulin (insB:9-23). Analysis of microbial protein sequences with homology to the insB:9-23 sequence revealed 17 peptides showing >50% identity to insB:9-23. Of these 17 peptides, the peptide, found in the normal human gut commensal , activated both human T cell clones from T1D patients and T cell hybridomas from nonobese diabetic (NOD) mice specific to insB:9-23. Immunization of NOD mice with insB:9-23 peptide mimic or insB:9-23 peptide verified immune cross-reactivity. Colonization of female NOD mice with accelerated the development of T1D, increasing macrophages, dendritic cells, and destructive CD8 T cells, while decreasing FoxP3 regulatory T cells. Western blot analysis identified -reacting antibodies in sera of NOD mice colonized with and human T1D patients. Furthermore, adoptive transfer of splenocytes from -treated mice to NOD/SCID mice enhanced disease phenotype in the recipients. Finally, analysis of human children gut microbiome data from a longitudinal DIABIMMUNE study revealed that seroconversion rates (i.e., the proportion of individuals developing two or more autoantibodies) were consistently higher in children whose microbiome harbored sequences capable of producing the peptide compared to individuals who did not harbor it. Taken together, these data demonstrate the potential role of a gut microbiota-derived insB:9-23-mimic peptide as a molecular trigger of T1D pathogenesis.
Topics: Animals; Autoantibodies; Bacteroidetes; CD8-Positive T-Lymphocytes; Child; Diabetes Mellitus, Type 1; Female; Gastrointestinal Microbiome; Humans; Insulin; Mice; Mice, Inbred NOD; Mice, SCID; Molecular Mimicry; Peptides
PubMed: 35878027
DOI: 10.1073/pnas.2120028119 -
Biomedical Journal Jun 2024The incidence of autoimmune diseases is increasing in developed countries, possibly due to the modern Western diet and lifestyle. We showed earlier that polysaccharides...
BACKGROUND
The incidence of autoimmune diseases is increasing in developed countries, possibly due to the modern Western diet and lifestyle. We showed earlier that polysaccharides derived from the medicinal fungus Hirsutella sinensis produced anti-inflammatory, anti-diabetic and anti-obesity effects by modulating the gut microbiota and increasing the abundance of the commensal Parabacteroides goldsteinii in mice fed with a high-fat diet.
METHODS
We examined the effects of the prebiotics, H. sinensis polysaccharides, and probiotic, P. goldsteinii, in a mouse model of imiquimod-induced systemic lupus erythematosus.
RESULTS
The fungal polysaccharides and P. goldsteinii reduced markers of lupus severity, including the increase of spleen weight, proteinuria, and serum levels of anti-DNA auto-antibodies and signal transducer and activator of transcription 4 (STAT4). Moreover, the polysaccharides and P. goldsteinii improved markers of kidney and liver functions such as creatinine, blood urea nitrogen, glomerulus damage and fibrosis, and serum liver enzymes. However, the prebiotics and probiotics did not influence gut microbiota composition, colonic histology, or expression of tight junction proteins in colon tissues.
CONCLUSIONS
Our results indicate that H. sinensis polysaccharides and the probiotic P. goldsteinii can reduce lupus markers in imiquimod-treated mice. These prebiotics and probiotics may therefore be added to other interventions conducive of a healthy lifestyle in order to counter autoimmune diseases.
PubMed: 38901796
DOI: 10.1016/j.bj.2024.100754 -
Frontiers in Nutrition 2024The intricate interplay between dietary habits and the development of Parkinson's Disease (PD) has long been a subject of scientific inquiry. Mendelian Randomization...
BACKGROUND
The intricate interplay between dietary habits and the development of Parkinson's Disease (PD) has long been a subject of scientific inquiry. Mendelian Randomization (MR) emerges as a potent tool, harnessing genetic variants to infer causality in observational data. While evidence links diet to Parkinson's Disease (PD) etiology, a thorough MR exploration of dietary impacts on PD, particularly involving gut microbiota, is still emerging.
METHODS
This research leverages the IEU Open GWAS project's vast GWAS database to address the knowledge gap in understanding diet's influence on PD, employing a diverse range of dietary variables. Our holistic dataset includes various foods like processed fava beans, bap, red wine, to cheese, reflecting a commitment to untangling dietary complexities in PD etiology. Advancing from initial dietary-PD associations, we innovatively explore the gut microbiota, focusing on in relation to bap intake and PD, employing MR. Utilizing weighted median, MR-Egger, and inverse variance weighting methods, we ensure rigorous causality assessments, meticulously mitigating pleiotropy and heterogeneity biases to uphold finding validity.
RESULTS
Our findings indicate red wine (OR: 1.031; 95% CI 1.001-1.062; = 0.044) and dried fruit consumption (OR: 2.019; 95% CI 1.052-3.875; = 0.035) correlate with increased PD risk, whereas broad beans (OR: 0.967; 95% CI 0.939-0.996; = 0.024) and bap intake (OR: 0.922; 95% CI 0.860-0.989; = 0.023) show protective effects against PD. Employing MR, specifically the IVW method, revealed a significant inverse association between bap intake and gut microbiota, marked by an 8.010-fold decrease in per standard deviation increase in bap intake (95% CI 1.005-63.818, = 0.049). Furthermore, a connection between PD and was observed (OR: 0.810; 95% CI 0.768-0.999; = 0.049), suggesting a potential microbiota-mediated pathway in PD etiology.
CONCLUSION
Our study links dietary habits to PD risk, showing higher PD risk with red wine and dried fruit consumption, and a protective effect from broad beans and bap. Using MR, we found bap intake inversely correlates with in the gut, suggesting bap influences microbiota. Further, higher levels correlate with lower PD risk, highlighting a complex interplay of diet, gut microbiome, and neurological health. These insights shed light on potential dietary interventions for PD.
PubMed: 38840699
DOI: 10.3389/fnut.2024.1273874 -
NPJ Biofilms and Microbiomes May 2023Cecal microbiota plays an essential role in chicken health. However, its contribution to fat metabolism, particularly in abdominal fat deposition, which is a severe...
Cecal microbiota plays an essential role in chicken health. However, its contribution to fat metabolism, particularly in abdominal fat deposition, which is a severe problem in the poultry industry, is still unclear. Here, chickens at 1, 4, and 12 months of age with significantly (p < 0.05) higher and lower abdominal fat deposition were selected to elucidate fat metabolism. A significantly (p < 0.05) higher mRNA expression of fat anabolism genes (ACSL1, FADS1, CYP2C45, ACC, and FAS), a significantly (p < 0.05) lower mRNA expression of fat catabolism genes (CPT-1 and PPARα) and fat transport gene APOAI in liver/abdominal fat of high abdominal fat deposition chickens indicated that an unbalanced fat metabolism leads to excessive abdominal fat deposition. Parabacteroides, Parasutterella, Oscillibacter, and Anaerofustis were found significantly (p < 0.05) higher in high abdominal fat deposition chickens, while Sphaerochaeta was higher in low abdominal fat deposition chickens. Further, Spearman correlation analysis indicated that the relative abundance of cecal Parabacteroides, Parasutterella, Oscillibacter, and Anaerofustis was positively correlated with abdominal fat deposition, yet cecal Sphaerochaeta was negatively correlated with fat deposition. Interestingly, transferring fecal microbiota from adult chickens with low abdominal fat deposition into one-day-old chicks significantly (p < 0.05) decreased Parabacteroides and fat anabolism genes, while markedly increased Sphaerochaeta (p < 0.05) and fat catabolism genes (p < 0.05). Our findings might help to assess the potential mechanism of cecal microbiota regulating fat deposition in chicken production.
Topics: Animals; Chickens; Lipid Metabolism; Microbiota; RNA, Messenger; Abdominal Fat
PubMed: 37253749
DOI: 10.1038/s41522-023-00390-8 -
Frontiers in Microbiology 2023The gut-lung axis has long been recognized as an important mechanism affecting intestinal and lung immunity. Still, few studies have examined the correlation between the...
INTRODUCTION
The gut-lung axis has long been recognized as an important mechanism affecting intestinal and lung immunity. Still, few studies have examined the correlation between the intestinal and pharyngeal microbiota in early neonates, especially when feeding patterns are one of the main drivers of microbiota development.
METHODS
To explore the composition and function of intestinal and pharyngeal microbiota and to analyze the effect of limited formula feeding on the initial microbiota colonization in early full-term neonates, we characterized the stool and oropharyngeal microbiota of 20 healthy full-term newborns sampled on days 0 and 5-7 after birth using 16S rRNA gene sequencing. Based on the sequencing results, a comparison was made of the compositions and functions of the intestinal and oropharyngeal microbiota for analysis.
RESULTS AND DISCUSSION
At the phylum level, , and were the most abundant in both niches. At the genus level, the species of pioneer bacteria were rich in the intestine and oropharynx but low in abundance on day 0. On days 5-7, (25.40%) and (22.16%) were dominant in the intestine, while (38.40%) and (23.13%) were dominant in the oropharynx. There were eight core bacteria genera in the intestine and oropharynx on days 5-7, which were , and . As indicated by PICRUSt analysis, on days 5-7, the intestinal microbiota was more predictive than the oropharyngeal microbiota in transcription, metabolism, cell motility, cellular processes and signaling, and organismal system function in the KEGG pathway. Compared to exclusive breastfeeding, limited formula feeding (40-60%) had no significant effect on the neonatal intestinal and oropharyngeal microbiota composition during the initial colonization period. Our results suggest that the initial colonization of microbiota is closely related to the ecological niche environment in the intestine and oropharynx, with their core microbiota being closely correlated. We found that early limited formula feeding could not significantly affect the initial colonization of microbiota in the intestine and oropharynx.
PubMed: 37601350
DOI: 10.3389/fmicb.2023.1225352 -
Heliyon Sep 2023This study aims to investigate the changes in gut microbiota and metabolism of patients with chronic kidney disease (CKD) stage 1-2, as well as the potential impact of...
OBJECT
This study aims to investigate the changes in gut microbiota and metabolism of patients with chronic kidney disease (CKD) stage 1-2, as well as the potential impact of hyperuricemia (HUA) on these factors in CKD stage 1-2 patients.
METHODS
In this study, fecal samples were collected from CKD stage 1-2 without HUA patients (CKD-N group), CKD stage 1-2 with HUA patients (CKD-H group), and healthy people controls (HCs group). The samples were then subjected to the microbiome (16S rRNA gene sequencing) and metabolome (liquid chromatography-tandem mass spectrometry) analyses. The multi-omics datasets were analyzed individually and integrated for combined analysis using various bioinformatics approaches.
RESULTS
Gut microbial dysbiosis was found in CKD-N and CKD-H patients. At the phylum level, compared to HCs group, decreased but increased in CKD-H group significantly. in CKD-N group was significantly lower than HCs group. At genus level, , , and significantly changed in CKD groups. was significantly lower in CKD-H group than CKD-N group. Moreover, the fecal metabolome of CKD-N and CKD-H altered significantly. d-glutamine and d-glutamate metabolism, arginine and proline metabolism, histidine metabolism, and lysine biosynthesis were down-regulated in the CKD-N group. Phenylalanine metabolism, arginine and proline metabolism, purine metabolism, and beta-alanine metabolism were up-regulated in the CKD-H group. There was a significant difference between the two CKD groups in phenylalanine metabolism. The abundance change of , , , , and had a close correlation with differential metabolites.
CONCLUSION
The gut microbiota and metabolic status undergo significant changes in CKD patients compared to healthy people. Additionally, HUA has been found to impact the gut microbiota of CKD patients, as well as their metabolism. The close association between gut microbiota and metabolites suggests that the former plays a crucial role in metabolism.
PubMed: 37809388
DOI: 10.1016/j.heliyon.2023.e20328 -
Microbiome May 2021The endoglycosidase heparanase which degrades heparan sulfate proteoglycans, exerts a pro-inflammatory mediator in various inflammatory disorders. However, the function...
BACKGROUND
The endoglycosidase heparanase which degrades heparan sulfate proteoglycans, exerts a pro-inflammatory mediator in various inflammatory disorders. However, the function and underlying mechanism of heparanase in acute pancreatitis remain poorly understood. Here, we investigated the interplay between heparanase and the gut microbiota in the development of acute pancreatitis.
METHODS
Acute pancreatitis was induced in wild-type and heparanase-transgenic mice by administration of caerulein. The differences in gut microbiota were analyzed by 16S ribosomal RNA sequencing. Antibiotic cocktail experiment, fecal microbiota transplantation, and cohousing experiments were used to assess the role of gut microbiota.
RESULTS
As compared with wild-type mice, acute pancreatitis was exacerbated in heparanase-transgenic mice. Moreover, the gut microbiota differed between heparanase-transgenic and wild-type mice. Heparanase exacerbated acute pancreatitis in a gut microbiota-dependent manner. Specially, the commensal Parabacteroides contributed most to distinguish the differences between wild-type and heparanase-transgenic mice. Administration of Parabacteroides alleviated acute pancreatitis in wild-type and heparanase-transgenic mice. In addition, Parabacteroides produced acetate to alleviate heparanase-exacerbated acute pancreatitis through reducing neutrophil infiltration.
CONCLUSIONS
The gut-pancreas axis played an important role in the development of acute pancreatitis and the acetate produced by Parabacteroides may be beneficial for acute pancreatitis treatment. Video abstract.
Topics: Acetates; Acute Disease; Animals; Bacteroides; Gastrointestinal Microbiome; Glucuronidase; Mice; Mice, Transgenic; Neutrophil Infiltration; Pancreatitis
PubMed: 34016163
DOI: 10.1186/s40168-021-01065-2 -
The Journal of Infectious Diseases Aug 2023Despite preventive measures, infections continue to pose significant risks to pediatric allogeneic hematopoietic cell transplantation (allo-HCT) recipients. The gut... (Observational Study)
Observational Study
BACKGROUND
Despite preventive measures, infections continue to pose significant risks to pediatric allogeneic hematopoietic cell transplantation (allo-HCT) recipients. The gut microbiota has been linked to clinical outcomes following adult allo-HCT. This study evaluated whether similar disruptions or differing microbiota patterns were associated with infection risk in pediatric allo-HCT.
METHODS
In a prospective observational study, fecal samples were obtained from 74 children before conditioning and upon neutrophil recovery. Microbiome signatures identified through sequencing were examined for their associations with infections or acute graft-versus-host disease (aGVHD) in the first-year post-HCT using Cox proportional hazards analysis.
RESULTS
Microbiome disruption in adults, did not predict infection risk in pediatric allo-HCT. Unique microbiota signatures were associated with different infections or aGVHD. A ratio of strict and facultative anaerobes (eg, Lachnoclostridium, Parabacteroides) prior to conditioning predicted bacteremia risk (Cox hazard ratio [HR], 3.89). A distinct ratio of oral (eg, Rothia, Veillonella) to intestinal anaerobes (eg, Anaerobutyricum, Romboutsia) at neutrophil recovery predicted likelihood of bacterial infections (Cox HR, 1.81) and viral enterocolitis (Cox HR, 1.96).
CONCLUSIONS
Interactions between medical interventions, pediatric hosts, and microbial communities contribute to microbiota signatures that predict infections. Further multicenter study is necessary to validate the generalizability of these ratios as biomarkers.
Topics: Adult; Humans; Child; Hematopoietic Stem Cell Transplantation; Bacteria; Feces; Gastrointestinal Microbiome; Graft vs Host Disease
PubMed: 37249910
DOI: 10.1093/infdis/jiad190 -
Frontiers in Nutrition 2022The purpose of this experiment was to investigate the effects of different starch and protein levels on lipid metabolism and gut microbes in mice of different genders. A...
The purpose of this experiment was to investigate the effects of different starch and protein levels on lipid metabolism and gut microbes in mice of different genders. A total of 160 male mice were randomly assigned to sixteen groups and fed a 4 × 4 Latin square design with dietary protein concentrations of 16, 18, 20, and 22%, and starch concentrations of 50, 52, 54, and 56%, respectively. The results of the study showed that different proportions of starch and protein had obvious effects on the liver index of mice, and there was a significant interaction between starch and protein on the liver index ( = 0.005). Compared with other protein ratio diets, 18% protein diet significantly increased the serum TBA concentration of mice ( < 0.001), and different starch ratio diets had no effect on serum TBA concentration ( = 0.442). It was proved from the results of ileal tissue HE staining that the low protein diet and the low starch diet were more favorable. There was a significant interaction between diets with different starch and protein levels on , and abundance in feces of mice ( < 0.001). Compared with 16 and 18% protein ratio diets, both 20 and 22% protein diets significantly decreased the and abundance in feces of mice ( < 0.05), and 52% starch ratio diet significantly decreased the and abundance than 50% starch ratio diet of mice ( < 0.05). There was a significant interaction between diets with different starch and protein levels on ( = 0.014) and ( = 0.001) abundance in feces of mice. Taken together, our results suggest that a low protein and starch diet can alter lipid metabolism and gut microbes in mice.
PubMed: 36466418
DOI: 10.3389/fnut.2022.1018026