scholarly journals Microbiota, Microbial Metabolites, and Barrier Function in A Patient with Anorexia Nervosa after Fecal Microbiota Transplantation

2019 ◽  
Vol 7 (9) ◽  
pp. 338 ◽  
Author(s):  
Prochazkova ◽  
Roubalova ◽  
Dvorak ◽  
Tlaskalova-Hogenova ◽  
Cermakova ◽  
...  

The change in the gut microbiome and microbial metabolites in a patient suffering from severe and enduring anorexia nervosa (AN) and diagnosed with small intestinal bacterial overgrowth syndrome (SIBO) was investigated. Microbial gut dysbiosis is associated with both AN and SIBO, and therefore gut microbiome changes by serial fecal microbiota transplantation (FMT) is a possible therapeutic modality. This study assessed the effects of FMT on gut barrier function, microbiota composition, and the levels of bacterial metabolic products. The patient treatment with FMT led to the improvement of gut barrier function, which was altered prior to FMT. Very low bacterial alpha diversity, a lack of beneficial bacteria, together with a great abundance of fungal species were observed in the patient stool sample before FMT. After FMT, both bacterial species richness and gut microbiome evenness increased in the patient, while the fungal alpha diversity decreased. The total short-chain fatty acids (SCFAs) levels (molecules presenting an important source of energy for epithelial gut cells) gradually increased after FMT. Contrarily, one of the most abundant intestinal neurotransmitters, serotonin, tended to decrease throughout the observation period. Overall, gut microbial dysbiosis improvement after FMT was considered. However, there were no signs of patient clinical improvement. The need for an in-depth analysis of the donor´s stool and correct selection pre-FMT is evident.

2021 ◽  
Vol 250 (1) ◽  
pp. X1
Author(s):  
Marion Régnier ◽  
Matthias Van Hul ◽  
Claude Knauf ◽  
Patrice D Cani

2019 ◽  
Vol 10 (3) ◽  
pp. 265-278 ◽  
Author(s):  
V. Stadlbauer ◽  
A. Horvath ◽  
I. Komarova ◽  
B. Schmerboeck ◽  
N. Feldbacher ◽  
...  

The gut is hypothesised to play an important role in the development and progression of sepsis. It is however unknown whether the gut microbiome and the gut barrier function is already altered early in sepsis development and whether it is possible to modulate the microbiome in early sepsis. Therefore, a randomised, double blind, placebo-controlled pilot study to examine the alterations of the microbiome and the gut barrier in early sepsis and the influence of a concomitant probiotic intervention on dysbiosis at this early stage of the disease was conducted. Patients with early sepsis, defined as fulfilling the sepsis definition from the 2012 Surviving Sepsis Campaign guidelines but without signs of organ failure, received multispecies probiotic (Winclove 607 based on Omnibiotic® 10 AAD) for 28 days. Gut microbiome composition, function, gut barrier and bacterial translocation were studied. Patients with early sepsis had a significantly lower structural and functional alpha diversity, clustered differently and showed structural alterations on all taxonomic levels. Gut permeability was unaltered but endotoxin, endotoxin binding proteins and peptidoglycans were elevated in early sepsis patients compared to controls. Probiotic intervention successfully increased probiotic strains in stool and led to an improvement of functional diversity. Microbiome composition and function are altered in early sepsis. Probiotic intervention successfully modulates the microbiome and is therefore a promising tool for early intervention in sepsis.


2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Giorgio Casaburi ◽  
Sercan Karav ◽  
Steve Frese ◽  
Bethany Henrick

Abstract Objectives The gut epithelium is single-celled barrier that employs many different mechanisms that together provide the first line of defense to physically separate the gut epithelium from our gut microbiome. Notably, the epithelial barrier is protected by a mucin layer providing a physical barrier limiting pathogen access to the epithelial monolayer. We sought to assess how changes in the gut microbiome resulting from colonization by a single strain of Bifidobacterium longum subsp. infantis EVC001 could alter gut barrier function. Methods Fecal samples from this trial were assessed for: (1) endotoxin (lipopolysaccharide) concentration; (2) functional contributions to the gut microbiome by shotgun metagenome sequencing; and (3) fecal glycan profiles by mass spectrometry to assess gut epithelial barrier integrity via breakdown of colonic mucin glycoproteins. Results Colonization with Bifidobacterium, including B. infantis EVC001, showed a significant four-fold reduction in fecal endoxtoxin levels and reductions in fecal inflammatory markers (P < 0.05). Shotgun metagenomics identified LPS-producing Enterobacteriaceae as the most significant contributor of virulence factors in the infant gut metagenome. These bacteria (primarily E. coli and Klebsiella spp.) were also significantly correlated with both mucolytic bacteria (e.g., Bacteroides) and the signatures of mucin breakdown, as assessed by mass spectrometric quantification of colonic mucin-derived glycans. Five different colonic-mucin specific glycans (3_1_1_0, 2_1_2_0, 2_1_1_1, 2_1_1_0, and 1_1_0_1) were significantly associated with microbiome composition (P < 0.05). Overall mucin glycans were inversely correlated with Bifidobacteriaceae abundance (Spearman's rho −0.66, FDR-corrected P value 0.04). Conclusions Complex interactions between the degradation of gut barrier function (e.g., mucin), the production of pro-inflammatory endotoxins, and the risk of infection by these bacteria coming in close contact with the gut epithelium suggest that B. infantis EVC001 can play a role in reducing these combined risks for neonates. Funding Sources This work was funded by Evolve Biosystems, Inc.


PLoS ONE ◽  
2019 ◽  
Vol 14 (2) ◽  
pp. e0211703 ◽  
Author(s):  
Vanessa Stadlbauer ◽  
Angela Horvath ◽  
Irina Komarova ◽  
Bianca Schmerboeck ◽  
Nicole Feldbacher ◽  
...  

2018 ◽  
Vol 132 (6) ◽  
pp. 701-718 ◽  
Author(s):  
Seungbum Kim ◽  
Ruby Goel ◽  
Ashok Kumar ◽  
Yanfei Qi ◽  
Gil Lobaton ◽  
...  

Recent evidence indicates a link between gut pathology and microbiome with hypertension (HTN) in animal models. However, whether this association exists in humans is unknown. Thus, our objectives in the present study were to test the hypotheses that high blood pressure (BP) patients have distinct gut microbiomes and that gut–epithelial barrier function markers and microbiome composition could predict systolic BP (SBP). Fecal samples, analyzed by shotgun metagenomics, displayed taxonomic and functional changes, including altered butyrate production between patients with high BP and reference subjects. Significant increases in plasma of intestinal fatty acid binding protein (I-FABP), lipopolysaccharide (LPS), and augmented gut-targetting proinflammatory T helper 17 (Th17) cells in high BP patients demonstrated increased intestinal inflammation and permeability. Zonulin, a gut epithelial tight junction protein regulator, was markedly elevated, further supporting gut barrier dysfunction in high BP. Zonulin strongly correlated with SBP (R2 = 0.5301, P<0.0001). Two models predicting SBP were built using stepwise linear regression analysis of microbiome data and circulating markers of gut health, and validated in a separate cohort by prediction of SBP from zonulin in plasma (R2 = 0.4608, P<0.0001). The mouse model of HTN, chronic angiotensin II (Ang II) infusion, was used to confirm the effects of butyrate and gut barrier function on the cardiovascular system and BP. These results support our conclusion that intestinal barrier dysfunction and microbiome function are linked to HTN in humans. They suggest that manipulation of gut microbiome and its barrier functions could be the new therapeutic and diagnostic avenues for HTN.


Viruses ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 1891
Author(s):  
Ronald J. Ellis ◽  
Jennifer E. Iudicello ◽  
Robert K. Heaton ◽  
Stéphane Isnard ◽  
John Lin ◽  
...  

People with human immunodeficiency virus (HIV) (PWH) have reduced gut barrier integrity (“leaky gut”) that permits diffusion of microbial antigens (microbial translocation) such as lipopolysaccharide (LPS) into the circulation, stimulating inflammation. A potential source of this disturbance, in addition to gut lymphoid tissue CD4+ T-cell depletion, is the interaction between the gut barrier and gut microbes themselves. We evaluated the relationship of gut barrier integrity, as indexed by plasma occludin levels (higher levels corresponding to greater loss of occludin from the gut barrier), to gut microbial diversity. PWH and people without HIV (PWoH) participants were recruited from community sources and provided stool, and 16S rRNA amplicon sequencing was used to characterize the gut microbiome. Microbial diversity was indexed by Faith’s phylogenetic diversity (PD). Participants were 50 PWH and 52 PWoH individuals, mean ± SD age 45.6 ± 14.5 years, 28 (27.5%) women, 50 (49.0%) non-white race/ethnicity. PWH had higher gut microbial diversity (Faith’s PD 14.2 ± 4.06 versus 11.7 ± 3.27; p = 0.0007), but occludin levels were not different (1.84 ± 0.311 versus 1.85 ± 0.274; p = 0.843). Lower gut microbial diversity was associated with higher plasma occludin levels in PWH (r = −0.251; p = 0.0111), but not in PWoH. A multivariable model demonstrated an interaction (p = 0.0459) such that the correlation between Faith’s PD and plasma occludin held only for PWH (r = −0.434; p = 0.0017), but not for PWoH individuals (r = −0.0227; p = 0.873). The pattern was similar for Shannon alpha diversity. Antiretroviral treatment and viral suppression status were not associated with gut microbial diversity (ps > 0.10). Plasma occludin levels were not significantly related to age, sex or ethnicity, nor to current or nadir CD4 or plasma viral load. Higher occludin levels were associated with higher plasma sCD14 and LPS, both markers of microbial translocation. Together, the findings suggest that damage to the gut epithelial barrier is an important mediator of microbial translocation and inflammation in PWH, and that reduced gut microbiome diversity may have an important role.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1990-P ◽  
Author(s):  
SHIHO FUJISAKA ◽  
ISAO USUI ◽  
ALLAH NAWAZ ◽  
YOSHIKO IGARASHI ◽  
TOMONOBU KADO ◽  
...  

Shock ◽  
2011 ◽  
Vol 35 (3) ◽  
pp. 275-281 ◽  
Author(s):  
Xiaofa Qin ◽  
Sharvil U. Sheth ◽  
Susan M. Sharpe ◽  
Wei Dong ◽  
Qi Lu ◽  
...  

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