Transition from infant- to adult-like gut microbiota.

Transition from an infant to an adult associated gut microbiota with age through establishment of strict anaerobic bacteria remains one of the key unresolved questions in gut microbial ecology. Here a comprehensive comparative analysis of stool microbiota in a large cohort of mothers and their children sampled longitudinally up until 2 years of age using sequencing analysis tool was presented that allows realistic microbial diversity estimates. In this work, evidence for the switch from children to adult associated microbial profile between 1 and 2 years of age was provided, suggestively driven by Bifidobacterium breve. An Operational Taxonomic Unit (OTU) belonging to B. breve was highly prevalent in the population throughout the first year of life, and was negatively associated with detection of a range of adult-like OTUs. Although an adult profile was not fully established by 2 years of age, it was demonstrated that with regards to the most prevalent OTUs, their prevalence in the child population by then already resembled that of the adult population. Taken together, it was proposed that late-colonizing OTUs were recruited at a later stage and were not acquired at birth with the recruitment being controlled by gatekeeping OTUs until the age of 1 year.

Deviations in human gut microbiota: a novel diagnostic test for determining dysbiosis in patients with IBS or IBD.

BACKGROUND: Dysbiosis is associated with many diseases, including irritable bowel syndrome (IBS), inflammatory bowel diseases (IBD), obesity and diabetes. Potential clinical impact of imbalance in the intestinal microbiota suggests need for new standardised diagnostic methods to facilitate microbiome profiling. AIM: To develop and validate a novel diagnostic test using faecal samples to profile the intestinal microbiota and identify and characterise dysbiosis. METHODS: Fifty-four DNA probes targeting ≥300 bacteria on different taxonomic levels were selected based on ability to distinguish between healthy controls and IBS patients in faecal samples. Overall, 165 healthy controls (normobiotic reference collection) were used to develop a dysbiosis model with a bacterial profile and Dysbiosis Index score output. The model algorithmically assesses faecal bacterial abundance and profile, and potential clinically relevant deviation in the microbiome from normobiosis. This model was tested in different samples from healthy volunteers and IBS and IBD patients (n = 330) to determine the ability to detect dysbiosis. RESULTS: Validation confirms dysbiosis was detected in 73% of IBS patients, 70% of treatment-naïve IBD patients and 80% of IBD patients in remission, vs. 16% of healthy individuals. Comparison of deep sequencing and the GA-map Dysbiosis Test, (Genetic Analysis AS, Oslo, Norway) illustrated good agreement in bacterial capture; the latter showing higher resolution by targeting pre-determined highly relevant bacteria. CONCLUSIONS: The GA-map Dysbiosis Test identifies and characterises dysbiosis in IBS and IBD patients, and provides insight into a patient's intestinal microbiota. Evaluating microbiota as a diagnostic strategy may allow monitoring of prescribed treatment regimens and improvement in new therapeutic approaches.

Correlation between the human fecal microbiota and depression.

BACKGROUND: Depression is a chronic syndrome with a pathogenesis linked to various genetic, biological, and environmental factors. Several links between gut microbiota and depression have been established in animal models. In humans, however, few correlations have yet been demonstrated. The aim of our work was therefore to identify potential correlations between human fecal microbiota (as a proxy for gut microbiota) and depression. METHODS: We analyzed fecal samples from 55 people, 37 patients, and 18 non-depressed controls. Our analyses were based on data generated by Illumina deep sequencing of 16S rRNA gene amplicons. KEY RESULTS: We found several correlations between depression and fecal microbiota. The correlations, however, showed opposite directions even for closely related Operational Taxonomic Units (OTU's), but were still associated with certain higher order phylogroups. The order Bacteroidales showed an overrepresentation (p = 0.05), while the family Lachnospiraceae showed an underrepresentation (p = 0.02) of OTU's associated with depression. At low taxonomic levels, there was one clade consisting of five OTU's within the genus Oscillibacter, and one clade within Alistipes (consisting of four OTU's) that showed a significant association with depression (p = 0.03 and 0.01, respectively). CONCLUSIONS & INFERENCES: The Oscillibacter type strain has valeric acid as its main metabolic end product, a homolog of neurotransmitter GABA, while Alistipes has previously been shown to be associated with induced stress in mice. In conclusion, the taxonomic correlations detected here may therefore correspond to mechanistic models.

Abrupt temporal fluctuations in the chicken fecal microbiota are explained by its gastrointestinal origin.

One of the main challenges in understanding the composition of fecal microbiota is that it can consist of microbial mixtures originating from different gastrointestinal (GI) segments. Here, we addressed this challenge for broiler chicken feces using a direct 16S rRNA gene-sequencing approach combined with multivariate statistical analyses. Broiler feces were chosen because of easy sampling and the importance for pathogen transmission to the human food chain. Feces were sampled daily for 16 days from chickens with and without a feed structure-induced stimulation of the gastric barrier function. Overall, we found four dominant microbial phylogroups in the feces. Two of the phylogroups were related to clostridia, one to lactobacilli, and one to Escherichia/Shigella. The relative composition of these phylogroups showed apparent stochastic temporal fluctuations in feces. Analyses of dissected chickens at the end of the experiment, however, showed that the two clostridial phylogroups were correlated to the microbiota in the cecum/colon and the small intestine, while the upper gut (crop and gizzard) microbiota was correlated to the lactobacillus phylogroup. In addition, chickens with a stimulated gizzard also showed less of the proximate GI dominating bacterial group in the feces, supporting the importance of the gastric barrier function. In conclusion, our results suggest that GI origin is a main determinant for the chicken fecal microbiota composition. This knowledge will be important for future understanding of factors affecting shedding of both harmful and beneficial gastrointestinal bacteria through feces.

Prevention of intestinal Campylobacter jejuni colonization in broilers by combinations of in-feed organic acids.

AIM: We have tested the effect of various combinations of formic acid and sorbate on Campylobacter jejuni colonization in broiler chickens to reduce the colonization of this zoonotic pathogen in broiler chicken flocks. METHODS AND RESULTS: Chickens were offered feed supplemented with different concentrations and combinations of formic acid and/or potassium sorbate. We found little or no effect on the Camp. jejuni colonization levels in chickens that were given feed supplemented with formic acid alone. A combination of 1.5% formic acid and 0.1% sorbate reduced the colonization of Camp. jejuni significantly, while a concentration of 2.0% formic acid in combination with 0.1% sorbate prevented Camp. jejuni colonization in chickens. This inhibition was replicated in two independent trials with a combination of three different Camp. jejuni strains. CONCLUSIONS: Our results show a novel and promising intervention strategy to reduce the incidence of Camp. jejuni in poultry products and to obtain safer food. SIGNIFICANCE AND IMPACT OF THE STUDY: To ensure food safety, a reduction of the carcass contamination with Camp. jejuni through reduced colonization of this pathogen in broiler chicken flocks is important. A range of organic acids as additives in feed and drinking water have already been evaluated for this purpose. However, no studies have yet shown a complete inhibition of Camp. jejuni colonization in broiler chickens.