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Marta Olivares Audrey M. Neyrinck Sarah A. Pötgens Martin Beaumont Nuria Salazar Patrice D. Cani Laure B. Bindels Nathalie M. Delzenne 《Diabetologia》2018,61(8):1838-1848
Aims/hypothesis
Dipeptidyl peptidase 4 (DPP-4) inhibitors are agents designed to increase the half-life of incretins. Although they are administered orally, little is known about their effects on the gut microbiota and functions, despite the fact that some bacteria present in the gut microbiota exhibit DPP-4-like activity. Our objective was to study the impact of the DPP-4 inhibitor vildagliptin on gut functions and the intestinal ecosystem in a murine model of obesity induced by a Western diet (WD).Methods
Twenty seven male C57BL/6J mice were randomised to receive a control diet, a WD (45% kJ from fat and 17% kJ from sucrose) or a WD + vildagliptin (0.6 mg/ml in drinking water) for 8 weeks.Results
Vildagliptin significantly reduced DPP-4 activity in the caecal content and faeces. Vildagliptin impacted on the composition of the gut microbiota and its metabolic activity. It mainly decreased Oscillibacter spp. (a direct effect independent of DPP-4 activity was shown on cultured O. valericigenes), increased Lactobacillus spp. and propionate, and reduced the ligands of Toll-like receptors 2 and 4. Vildagliptin protected against the reductions in crypt depth and ileal expression of antimicrobial peptides induced by the WD. In the liver, the expression of immune cell populations (Cd3g and Cd11c [also known as Itgax]) and cytokines was decreased in the WD + vildagliptin-fed mice compared with the WD-fed group. Ex vivo exposure of precision-cut liver slices to vildagliptin showed that this response was not related to a direct effect of the drug on the liver tissue.Conclusions/interpretation
Our study is the first to consider the DPP-4-like activity of the gut microbiota as a target of DPP-4 inhibition. We propose that vildagliptin exerts beneficial effects at the intestinal level in association with modulation of gut microbiota, with consequences for hepatic immunity. If relevant in humans, this could open new therapeutic uses of DPP-4 inhibition to tackle gut dysfunctions in different pathophysiological contexts.Data availability
The sequences used for analysis can be found in the MG-RAST database under the project name MYNEWGUT3.2.
Zhou Feng Wenmin Long Binhan Hao Ding Ding Xiaoqing Ma Liping Zhao Xiaoyan Pang 《Gut pathogens》2017,9(1):59
Background
Bilophila wadsworthia is a major member of sulfidogenic bacteria in human gut, it was originally recovered from different clinical specimens of intra-abdominal infections and recently was reported potentially linked to different chronic metabolic disorders. However, there is still insufficient understanding on its detailed function and mechanism to date.Methods
A B. wadsworthia strain was isolated from fresh feces of a latent autoimmune diabetes in adults patient and we investigated its pathogenicity by oral administration to specific-pathogen-free mice. Tissue samples and serum were collected after sacrifice. Stool samples were collected at different time points to profile the gut microbiota.Results
Bilophila wadsworthia infection resulted in the reduction of body weight and fat mass, apparent hepatosplenomegaly and elevated serum inflammatory factors, including serum amyloid A and interleukin-6, while without significant change of the overall gut microbiota structure.Conclusions
These results demonstrated that higher amount of B. wadsworthia caused systemic inflammatory response in SPF mice, which adds new evidence to the pathogenicity of this bacterium and implied its potential role to the chronic inflammation related metabolic diseases like diabetes.3.
Vincent Blasco-Baque Berengère Coupé Aurelie Fabre Sandra Handgraaf Pierre Gourdy Jean-François Arnal Michael Courtney Carole Schuster-Klein Beatrice Guardiola François Tercé Rémy Burcelin Matteo Serino 《Diabetologia》2017,60(4):690-700
Aims/hypothesis
Despite the current pandemic of metabolic diseases, our understanding of the diverse nature of the development of metabolic alterations in people who eat a high-fat diet (HFD) is still poor. We recently demonstrated a cardio-metabolic adaptation in mice fed an HFD, which was characterised by a specific gut and periodontal microbiota profile. Since the severity of hepatic disease is characterised by specific microRNA (miRNA) signatures and the gut microbiota is a key driver of both hepatic disease and miRNA expression, we analysed the expression of three hepatic miRNA and studied their correlation with hepatic triacylglycerol content and gut microbiota.Methods
Two cohorts of C57BL/6 4-week-old wild-type (WT) male mice (n?=?62 and n?=?96) were fed an HFD for 3 months to provide a model of metabolic adaptation. Additionally 8-week-old C57BL/6 mice, either WT or of different genotypes, with diverse gut microbiota (ob/ob, Nod1, Cd14 knockout [Cd14KO] and Nod2) or without gut microbiota (axenic mice) were fed a normal chow diet. Following which, glycaemic index, body weight, blood glucose levels and hepatic triacylglycerol levels were measured. Gut (caecum) microbiota taxa were analysed by pyrosequencing. To analyse hepatic miRNA expression, real-time PCR was performed on total extracted miRNA samples. Data were analysed using two-way ANOVA followed by the Dunnett’s post hoc test, or by the unpaired Student’s t test. A cluster analysis and multivariate analyses were also performed.Results
Our results demonstrated that the expression of miR-181a, miR-666 and miR-21 in primary murine hepatocytes is controlled by lipopolysaccharide in a dose-dependent manner. Of the gut microbiota, Firmicutes were positively correlated and Proteobacteria and Bacteroides acidifaciens were negatively correlated with liver triacylglycerol levels. Furthermore, the relative abundance of Firmicutes was negatively correlated with hepatic expression of miR-666 and miR-21. In contrast, the relative abundance of B. acidifaciens was positively correlated with miR-21.Conclusions/interpretation
We propose the involvement of hepatic miRNA, liver triacylglycerols and gut microbiota as a new triad that underlies the molecular mechanisms by which gut microbiota governs hepatic pathophysiology during metabolic adaptation to HFD.4.
Xiuli Xiao Wenbo Long Tingyu Huang Tian Xia Rupei Ye Yong Liu Hanan Long 《Digestive diseases and sciences》2018,63(11):2923-2929
Background
Multiple factors including host–microbiota interaction could contribute to the conversion of healthy mucosa to sporadic precancerous lesions. An imbalance of the gut microbiota may be a cause or consequence of this process.Aim
The goal was to investigate and analyze the composition of gut microbiota during the genesis of precancerous lesions of colorectal cancer.Methods
To analyze the composition of gut microbiota in the genesis of precancerous lesions, a rat model of 1, 2-dimethylhydrazine (DMH)-induced aberrant crypt foci (ACF) was established. The feces of these rats and healthy rats were collected for 16S rRNA sequencing.Results
The diversity and density of the rat intestinal microbiota were significantly different between ACF-bearing and non-bearing group. ACF were induced in rats treated with DMH and showed increased expression of the inflammatory cytokines IL-6, IL-8, and TNF-α. Firmicutes was the most predominant phylum in both ACF-bearing and non-bearing group, followed by Bacteroidetes. Interestingly, although the density of Bacteroidetes decreased from the fifth week to the 17th week in both groups, it was significantly reduced in ACF-bearing group at the 13th week (P?<?0.01). At the genus level, no significant difference was observed in the most predominant genus, Lactobacillus. Instead, Bacteroides and Prevotella were significantly less abundant (P?<?0.01), while Akkermansia was significantly more abundant (P?<?0.05) in ACF-bearing group at the 13th week.Conclusion
Imbalance of the intestinal microbiota existed between ACF-bearing and non-bearing rats, which could be used as biomarker to predict the genesis of precancerous lesions in the gut.5.
Omar Youssef Leo Lahti Arto Kokkola Tiina Karla Milja Tikkanen Homa Ehsan Monika Carpelan-Holmström Selja Koskensalo Tom Böhling Hilpi Rautelin Pauli Puolakkainen Sakari Knuutila Virinder Sarhadi 《Digestive diseases and sciences》2018,63(11):2950-2958
Background
Microbial ecosystems that inhabit the human gut form central component of our physiology and metabolism, regulating and modulating both health and disease. Changes or disturbances in the composition and activity of this gut microbiota can result in altered immunity, inflammation, and even cancer.Aim
To compare the composition and diversity of gut microbiota in stool samples from patient groups based on the site of neoplasm in the gastrointestinal tract (GIT) and to assess the possible contribution of the bacterial composition to tumorigenesis.Methods
We studied gut microbiota by16S RNA gene sequencing from stool DNA of 83 patients, who were diagnosed with different GIT neoplasms, and 13 healthy individuals.Results
As compared to healthy individuals, stools of patients with stomach neoplasms had elevated levels of Enterobacteriaceae, and those with rectal neoplasms had lower levels of Bifidobacteriaceae. Lower abundance of Lactobacillaceae was seen in patients with colon neoplasms. Abundance of Lactobacillaceae was higher in stools of GIT patients sampled after cancer treatment compared to samples collected before start of any treatment. In addition to site-specific differences, higher abundances of Ruminococcus, Subdoligranulum and lower abundances of Lachnoclostridium and Oscillibacter were observed in overall GIT neoplasms as compared to healthy controlsConclusion
Our study demonstrates that the alterations in gut microbiota vary according to the site of GIT neoplasm. The observed lower abundance of two common families, Lactobacillaceae and Bifidobacteriaceae, and the increased abundance of Enterobacteriaceae could provide indicators of compromised gut health and potentially facilitate GIT disease monitoring.6.
Purpose of Review
Obesity and diabetes are worldwide epidemics. There is also a growing body of evidence relating the gut microbiome composition to insulin resistance. The purpose of this review is to delineate the studies linking gut microbiota to obesity, metabolic syndrome, and diabetes.Recent findings
Animal studies as well as proof of concept studies using fecal transplantation demonstrate the pivotal role of the gut microbiota in regulating insulin resistance states and inflammation.Summary
While we still need to standardize methodologies to study the microbiome, there is an abundance of evidence pointing to the link between gut microbiome, inflammation, and insulin resistance, and future studies should be aimed at identifying unifying mechanisms.7.
Purpose of Review
Accumulating evidence suggests that gut microbiota affect the development and function of the immune system and may play a role in the pathogenesis of autoimmune diseases. The purpose of this review is to summarize recent studies reporting gastrointestinal microbiota aberrations associated with the systemic sclerosis disease state.Recent Findings
The studies described herein have identified common changes in gut microbial composition. Specifically, patients with SSc have decreased abundance of beneficial commensal genera (e.g., Faecalibacterium, Clostridium, and Bacteroides) and increased abundance of pathobiont genera (e.g., Fusobacterium, Prevotella, Erwinia). In addition, some studies have linked specific genera with the severity of gastrointestinal symptoms in systemic sclerosis.Summary
More research is needed to further characterize the gastrointestinal microbiota in systemic sclerosis and understand how microbiota perturbations can affect inflammation, fibrosis, and clinical outcomes. Interventional studies aimed at addressing/correcting these perturbations, either through dietary modification, pro/pre-biotic supplementation, or fecal transplantation, may lead to improved outcomes for patients with systemic sclerosis.8.
Background
Recent advances in next-generation sequencing technologies have enabled comprehensive analysis of the gut microbiota, which is closely linked to the health of the host. Consequently, several studies have explored the factors affecting gut microbiota composition. In recent years, increasing number of dog owners are feeding their pets a natural diet i.e., one consisting of bones, raw meat (such as chicken and beef), and vegetables, instead of commercial feed. However, the effect of these diets on the microbiota of dogs (Canis lupus familiaris) is unclear.Methods and results
Six dogs fed a natural diet and five dogs fed a commercial feed were selected; dog fecal metagenomic DNA samples were analyzed using the Illumina MiSeq platform. Pronounced differences in alpha and beta diversities, and taxonomic composition of the core gut microbiota were observed between the two groups. According to alpha diversity, the number of operational taxonomic units, the richness estimates, and diversity indices of microbiota were significantly higher (p < 0.05) in the natural diet group than in the commercial feed group. Based on beta diversity, most samples clustered together according to the diet type (p = 0.004). Additionally, the core microbiota between the two groups was different at the phylum, family, and species levels. Marked differences in the taxonomic composition of the core microbiota of the two groups were observed at the species level; Clostridium perfringens (p = 0.017) and Fusobacterium varium (p = 0.030) were more abundant in the natural diet group.Conclusions
The gut microbiota of dogs is significantly influenced by diet type (i.e., natural diet and commercial feed). Specifically, dogs fed a natural diet have more diverse and abundant microbial composition in the gut microbiota than dogs fed a commercial feed. In addition, this study suggests that in dogs fed a natural diet, the potential risk of opportunistic infection could be higher, than in dogs fed a commercial feed. The type of diet might therefore play a key role in animal health by affecting the gut microbiota. This study could be the basis for future gut microbiota research in dogs.9.
Rossana Rosa Curtis J. Donskey L. Silvia Munoz-Price 《Current infectious disease reports》2018,20(8):27
Purpose of Review
Colonization resistance refers to the innate defense provided by the indigenous microbiota against colonization by pathogenic organisms. We aim to describe how this line of defense is deployed against Clostridium difficile and what the implications are for interventions directed by Antimicrobial Stewardship Programs.Recent Findings
The indigenous microbiota provides colonization resistance through depletion of nutrients, prevention of access to adherence sites within the gut mucosa, production of inhibitory substances, and stimulation of the host’s immune system. The ability to quantify colonization resistance could provide information regarding periods of maximal vulnerability to colonization with pathogens and also allow the identification of mechanisms of restoration of colonization resistance. Methods utilized to determine the composition of the gut microbiota include sequencing technologies and measurement of concentration of specific bacterial metabolites.Summary
Use of innovations in the quantification of colonization resistance can expand the role of Antimicrobial Stewardship from prevention of disruption of the indigenous microbiota to restoration of colonization resistance.10.
Background
The intestinal microbiome plays an essential role in the development of chronic inflammatory diseases, such as inflammatory bowel disease (IBD) or metabolic disorders.Objectives
What is the pathophysiological role of the intestine as an interface between bacterial and host functions?Methods
Recent findings related to intestinal function and microbe–host interactions in the context of inflammatory and metabolic disorders are reviewed.Results and conclusions
Changes in gut microbiota composition and function (dysbiosis) are associated with a variety of different pathologies. Dysbiosis in combination with the loss of gut barrier and immune functions are shared in inflammatory and metabolic disorders. Causal mechanisms for the interaction of dysbiotic microbial communities in the gut and disease onset require additional clinical and experimental validation including prospective cohort and gnotobiotic animal studies. Fecal microbiota transplantation and targeted microbial therapies are promising strategies for clinical intervention; however many questions need to be addressed including disease-specific selection of donor microbiota or synthetic bacterial consortia, application strategies and risk evaluation.11.
Lena M. Biehl Rebeca Cruz Aguilar Fedja Farowski Werner Hahn Angela Nowag Hilmar Wisplinghoff Maria J. G. T. Vehreschild 《Infection》2018,46(6):871-874
Purpose
We report on a kidney transplant recipient treated with fecal microbiota transplantation (FMT) for recurrent urinary tract infections.Methods
FMT was administered via frozen capsulized microbiota. Before and after FMT, urinary, fecal and vaginal microbiota compositions were analyzed.Results
The patient remained without symptoms after FMT.Conclusions
Underlying mechanisms of action need to be addressed in depth by future research.12.
Purpose of Review
The objective of this review is to critically assess the contributing role of the gut microbiota in human obesity and type 2 diabetes (T2D).Recent Findings
Experiments in animal and human studies have produced growing evidence for the causality of the gut microbiome in developing obesity and T2D. The introduction of high-throughput sequencing technologies has provided novel insight into the interpersonal differences in microbiome composition and function.Summary
The intestinal microbiota is known to be associated with metabolic syndrome and related comorbidities. Associated diseases including obesity, T2D, and fatty liver disease (NAFLD/NASH) all seem to be linked to altered microbial composition; however, causality has not been proven yet. Elucidating the potential causal and personalized role of the human gut microbiota in obesity and T2D is highly prioritized.13.
Mariko Hojo Takashi Asahara Akihito Nagahara Tsutomu Takeda Kohei Matsumoto Hiroya Ueyama Kenshi Matsumoto Daisuke Asaoka Takuya Takahashi Koji Nomoto Yuichiro Yamashiro Sumio Watanabe 《Digestive diseases and sciences》2018,63(11):2940-2949
Background
Recently, problems associated with proton pump inhibitor (PPI) use have begun to surface. PPIs influence the gut microbiota; therefore, PPI use may increase the risk of enteric infections and cause bacterial translocation. In this study, we investigated fecal microbiota composition, fecal organic acid concentrations and pH, and gut bacteria in the blood of the same patients before and after PPI use.Methods
Twenty patients with reflux esophagitis based on endoscopic examination received 8 weeks of treatment with PPIs. To analyze fecal microbiota composition and gut bacteria in blood and organic acid concentrations, 16S and 23S rRNA-targeted quantitative RT-PCR and high-performance liquid chromatography were conducted.Results
Lactobacillus species were significantly increased at both 4 and 8 weeks after PPI treatment compared with bacterial counts before treatment (P?=?0.011 and P?=?0.002, respectively). Among Lactobacillus spp., counts of the L. gasseri subgroup, L. fermentum, the L. reuteri subgroup, and the L. ruminis subgroup were significantly increased at 4 and 8 weeks after treatment compared with counts before treatment. Streptococcus species were also significantly increased at 4 and 8 weeks after PPI treatment compared with counts before treatment (P?<?0.01 and P?<?0.001, respectively). There was no significant difference in the total organic acid concentrations before and after PPI treatment. Detection rates of bacteria in blood before and after PPI treatment were 22 and 28%, respectively, with no significant differences.Conclusions
Our quantitative RT-PCR results showed that gut dysbiosis was caused by PPI use, corroborating previous results obtained by metagenomic analysis.14.
Elke Gülden 《Current diabetes reports》2018,18(11):111
Purpose of Review
The incidence of type 1 diabetes (T1D) is rising drastically for the past decades at a rate that cannot be explained by genetic changes alone. Environmental changes are considered to be the main drivers of this change. Recently, the gut microbiota has been suggested as a missing link between known environmental disease modulators and T1D promotion. Lifestyle factors have changed over time and have altered the gut microbiota-host interaction affecting T1D development. The purpose of this review is to discuss recent data emphasizing the modulatory potential of early lifestyle factors on gut microbiota and to elucidate their implication for T1D.Recent Findings
Recent findings show that lifestyle factors, especially those that affect the early establishment of gut homeostasis and the education of the immune system, are crucial disease modulators.Summary
Changing lifestyle factors affecting the early establishment of gut homeostasis are suggested to be key drivers of the rising T1D incidence.15.
Background
The gut microbiome has emerged as a key player in the modulation of the immune system and metabolism. Changes in the composition of the gut microbial ecosystems have been reported to be associated with metabolic diseases but also with the development and progression of cardiovascular diseases, inflammatory bowel disease, certain types of cancer and psychiatric diseases.Objective
The role of the gut microbiome in the pathophysiology of obesity and type 2 diabetes, and treatment approaches based thereon are discussed.Microbiome and pathophysiology
The pathophysiology in humans is not entirely understood. Studies in mice suggest a strong causal link between changes in the microbiome and the development of metabolic diseases. Potential mechanisms how the microbiome is linked to diseases of the host include signaling through lipopolysaccharides from gram-negative bacteria and interactions with the host immune system, fermentation of indigestible fiber to short chain fatty acids, modulation of bile acids, and bile acid signaling. Interactions between gut microbiota, its products, and the immune system may lead to an increased gut permeability resulting in visceral fat and liver inflammation with subsequent systemic subclinical inflammation (leaky gut hypothesis). Moreover, host-specific factors and environmental factors have been discussed to have a role.Conclusion
Increasing knowledge in this area could contribute to the treatment of obesity and type 2 diabetes with fecal or targeted microbiota transplantation.16.
Antonio Sircana Luciana Framarin Nicola Leone Mara Berrutti Francesca Castellino Renato Parente Franco De Michieli Elena Paschetta Giovanni Musso 《Current diabetes reports》2018,18(10):98
Purpose of Review
In the last decade many studies have suggested an association between the altered gut microbiota and multiple systemic diseases including diabetes. In this review, we will discuss potential pathophysiological mechanisms, the latest findings regarding the mechanisms linking gut dysbiosis and type 2 diabetes (T2D), and the results obtained with experimental modulation of microbiota.Recent Findings
In T2D, gut dysbiosis contributes to onset and maintenance of insulin resistance. Different strategies that reduce dysbiosis can improve glycemic control.Summary
Evidence in animals and humans reveals differences between the gut microbial composition in healthy individuals and those with T2D. Changes in the intestinal ecosystem could cause inflammation, alter intestinal permeability, and modulate metabolism of bile acids, short-chain fatty acids and metabolites that act synergistically on metabolic regulation systems contributing to insulin resistance. Interventions that restore equilibrium in the gut appear to have beneficial effects and improve glycemic control. Future research should examine in detail and in larger studies other possible pathophysiological mechanisms to identify specific pathways modulated by microbiota modulation and identify new potential therapeutic targets.17.
Stefan G. Kertesz Erika Laine Austin Sally K. Holmes David E. Pollio Joseph E. Schumacher Bert White Carol VanDeusen Lukas 《Journal of general internal medicine》2014,29(4):835-844
BACKGROUND
While most organizational literature has focused on initiatives that transpire inside the hospital walls, the redesign of American health care increasingly asks that health care institutions address matters outside their walls, targeting the health of populations. The US Department of Veterans Affairs (VA)’s national effort to end Veteran homelessness represents an externally focused organizational endeavor.OBJECTIVE
Our aim was to evaluate the role of organizational practices in the implementation of Housing First (HF), an evidence-based homeless intervention for chronically homeless individuals.DESIGN
This was an interview-based comparative case study conducted across eight VA Medical Centers (VAMCs).PARTICIPANTS
Front line staff, mid-level managers, and senior leaders at VA Medical Centers were interviewed between February and December 2012.APPROACH
Using a structured narrative and numeric scoring, we assessed the correlation between successful HF implementation and organizational practices devised according to the organizational transformation model (OTM).KEY RESULTS
Scoring results suggested a strong association between HF implementation and OTM practice. Strong impetus to house Veterans came from national leadership, reinforced by Medical Center directors closely tracking results. More effective Medical Center leaders differentiated themselves by joining front-line staff in the work (at public events and in process improvement exercises), by elevating homeless-knowledgeable persons into senior leadership, and by exerting themselves to resolve logistic challenges. Vertical alignment and horizontal integration advanced at sites that fostered work groups cutting across service lines and hierarchical levels. By contrast, weak alignment from top to bottom typically also hindered cooperation across departments. Staff commitment to ending homelessness was high, though sustainability planning was limited in this baseline year of observation.CONCLUSION
Key organizational practices correlated with more successful implementation of HF for homeless Veterans. Medical Center directors substantively influenced the success of this endeavor through their actions to foster impetus, demonstrate commitment and support alignment and integration.18.
Purpose of Review
The microbiome is the term that describes the microbial ecosystem that cohabits an organism such as humans. The microbiome has been implicated in a long list of immune-mediated diseases which include rheumatoid arthritis, ankylosing spondylitis, and even gout. The mechanisms to account for this effect are multiple. The clinical implications from observations on the microbiome and disease are broad.Recent Findings
A growing number of microbiota constituents such as Prevotella copri, Porphyromonas gingivalis, and Collinsella have been correlated or causally related to rheumatic disease. The microbiome has a marked effect on the immune system. Our understanding of immune pathways modulated by the microbiota such as the induction of T helper 17 (Th17) cells and secretory immunoglobulin A (IgA) responses to segmented filamentous bacteria continues to expand. In addition to the gut microbiome, bacterial communities of other sites such as the mouth, lung, and skin have also been associated with the pathogenesis of rheumatic diseases.Summary
Strategies to alter the microbiome or to alter the immune activation from the microbiome might play a role in the future therapy for rheumatic diseases.19.
Trine B. Rounge Roger Meisal Jan Inge Nordby Ole Herman Ambur Thomas de Lange Geir Hoff 《BMC gastroenterology》2018,18(1):171
Background
Associations between colorectal cancer and microbiota have been identified. Archived fecal samples might be valuable sample sources for investigating causality in carcinogenesis and biomarkers discovery due to the potential of performing longitudinal studies. However, the quality, quantity and stability of the gut microbiota in these fecal samples must be assessed prior to such studies. We evaluated i) cross-contamination during analysis for fecal blood and ii) evaporation in stored perforated fecal immunochemical tests (iFOBT) samples, iii) temperature stability as well as iv) comparison of the gut microbiota diversity and composition in archived, iFOBT and fresh fecal samples in order to assess feasibility of large scale microbiota studies.Methods
The microbiota profiles were obtained by sequencing the V3-V4 region of 16S rDNA gene.Results
The iFOBT does not introduce any cross-sample contamination detectable by qPCR. Neither could we detect evaporation during freeze-thaw cycle of perforated iFOBT samples. Our results confirm room temperature stability of the gut microbiome. Diverse microbial profiles were achieved in 100% of fresh, 81% of long-term archived and 96% of iFOBT samples. Microbial diversity and composition were comparable between fresh and iFOBT samples, however, diversity differed significantly between long-term archived, fresh and iFOBT samples.Conclusion
Our data showed that it is feasible to exploit archived fecal sample sets originally collected for testing of fecal blood. The advantages of using these sample sets for microbial biomarker discovery and longitudinal observational studies are the availability of high-quality diagnostic and follow-up data. However, care must be taken when microbiota are profiled in long-term archived fecal samples.20.