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Colonization of breastfed infants by Bifidobacterium longum subsp. infantis EVC001 reduces virulence gene abundance

The infant gut microbiome is rapidly colonized by bacteria from the environment after birth, and this gut ecosystem can facilitate expansion of potential pathogens. Human milk shapes the infant gut microbiome and has evolved to foster the growth of specific bacteria. Breastfed infants fed the coevolved infant gut symbiont Bifidobacterium longum subsp. infantis EVC001 had significant modifications to their gut metagenome, including a decreased number of virulence factor genes

Integrating the Ecosystem Services Framework to Define Dysbiosis of the Breastfed Infant Gut: The Role of B. infantis and Human Milk Oligosaccharides

Mounting evidence supports a connection between the composition of the infant gut microbiome and long-term health. In fact, aberrant microbiome compositions during key developmental windows in early life are associated with increased disease risk; therefore, making pertinent modifications to the microbiome during infancy offers significant promise to improve human health. There is growing support for integrating the concept of ecosystem services (the provision of benefits from ecosystems to humans) in linking specific microbiome functions to human well-being. This framework is widely applied in conservation efforts of macro-ecosystems and offers a systematic approach to guide restoration actions aimed to recover critical ecological functions. The aim of this work is to apply the ecosystem services framework to integrate recent studies demonstrating stable alteration of the gut microbiome of breastfed infants when Bifidobacterium longum subsp. infantis EVC001, a gut symbiont capable of efficiently utilizing human milk oligosaccharides into organic acids that are beneficial for the infant and lower intestinal pH, is reintroduced. Additionally, using examples from the literature we illustrate how the absence of B. infantis results in diminished ecosystem services, which may be associated with health consequences related to immune and metabolic disorders. Finally, we propose a model by which infant gut dysbiosis can be defined as a reduction in ecosystem services supplied to the host by the gut microbiome rather than merely changes in diversity or taxonomic composition. Given the increased interest in targeted microbiome modification therapies to decrease acute and chronic disease risk, the model presented here provides a framework to assess the effectiveness of such strategies from a host-centered perspective

Reduced colonic mucin degradation in breastfed infants colonized by \u3ci\u3eBifidobacterium longum\u3c/i\u3e subsp. \u3ci\u3einfantis\u3c/i\u3e EVC001

Mucin glycoproteins play an important role in protecting the gut epithelium by keeping gut microbes from direct contact with the gut epithelium while allowing for diffusion of small molecules from the lumen to the epithelium. The mucin glycocalyx can be degraded by gut bacteria such as Bacteroides and Akkermansia, but other bacteria, such as Bifidobacterium longum subsp. Infantis, cannot consume mucin glycans. Untargeted mass spectrometry profiles were compared to microbiome profiles to assess how different gut microbiomes affect colonic mucin degradation. Samples obtained from nine infants colonized by Bifidobacterium infantis EVC001 and from 10 infants colonized by higher levels of mucolytic taxa (controls), including Bacteroides, were compared. Previously performed untargeted nano-high-performance liquid chromatography-chip/time-of-flight mass spectrometry was used to detect and quantify glycans originating from colonic mucin. Colonic mucin-derived O-glycans from control infants composed 37.68% (± 3.14% SD) of the total glycan structure pool, whereas colonic mucin-derived O-glycans made up of only 1.78% (± 0.038% SD) of the total in B. infantis EVC001 samples. The relative abundance of these colonic mucin-derived O-glycans in the total glycan pool was higher among control, 26.98% (± 8.48% SD), relative to B. infantis-colonized infants, 1.68% (± 1.12% SD). Key taxa, such as Bacteroidaceae, were significantly and positively correlated with the abundance of these structures, while Bifidobacteriaceae were significantly and negatively associated with these structures. These results suggest that colonization of infants by B. infantis may diminish colonic glycan degradation and help maintain barrier function in the gastrointestinal tract of infants

N-glycans from human milk glycoproteins are selectively released by an infant gut symbiont in vivo

Complex, indigestible free oligosaccharides as well as conjugated glycans are found in milk that shape the gut microbiome of infants. The activity of an endo-β-N-acetylglucosaminidase from B. longum subsp. infantis (B. infantis) is known to release N-glycans from native milk glycoproteins under physiological conditions. We investigated whether this enzyme is active in vivo in breastfed infants fed B. infantis EVC001. Using mass spectrometry, we found 19 N-glycans related to human milk glycoproteins increased in abundance, similar to previous work using bovine milk glycoproteins, and these 19 N-glycans matched unique specificities of this enzyme. Twenty N-glycans were unique to infants fed B. infantis EVC001. Bifidobacteriaceae were correlated with these glycans, confirming the relationship between B. infantis and released N-glycans. This suggests that this enzyme is active in vivo and releases N-glycans from milk glycoproteins, and may play a role in B. infantis EVC001 colonization of the gut microbiome

A common microbial signature is present in the lower airways of interstitial lung diseases including sarcoidosis

Background: The etiology of pulmonary sarcoidosis is not well established. Although the mechanism triggering pulmonary sarcoidosis remains to be established, inflammatory reactions seem to play an important role in this process. Objectives: The aim of this study was to define the composition of the lower airway microbiota in the bronchoalveolar lavage (BAL) of patients affected by interstitial lung diseases, including sarcoidosis, to determine whether the bacterial signature differs among these diseases. Methods: Ten patients affected by pulmonary sarcoidosis and 9 patients affected by other interstitial lung diseases were enrolled. 16S rRNA next-generation sequencing was used to study BAL microbial composition of these patients, and were also compared with already published microbial content in higher airways of such diseases. Results: Four phyla dominated the lower airway microbiota, Bacteroidetes being the most abundant phylum in both groups (56.9%). Diversity analysis showed no significant differences between the various diseases, particularly between pulmonary sarcoidosis and other interstitial lung diseases affecting lower airways. Conclusions: Our data indicate that the bacterial lower airways microbiota share the same signature and, therefore, cannot be used as a diagnostic tool to discriminate among different interstitial lung diseases, including sarcoidosis, while microbial diversity is present when considering lower or higher respiratory airways

Comparative Genome Analysis of Bifidobacterium longum subsp. infantis Strains Reveals Variation in Human Milk Oligosaccharide Utilization Genes among Commercial Probiotics

Dysbiosis is associated with acute and long-term consequences for neonates. Probiotics can be effective in limiting the growth of bacteria associated with dysbiosis and promoting the healthy development of the infant microbiome. Given its adaptation to the infant gut, and promising data from animal and in vitro models, Bifidobacterium longum subsp. infantis is an attractive candidate for use in infant probiotics. However, strain-level differences in the ability of commercialized strains to utilize human milk oligosaccharides (HMOs) may have implications in the performance of strains in the infant gut. In this study, we characterized twelve B. infantis probiotic strains and identified two main variants in one of the HMO utilization gene clusters. Some strains possessed the full repertoire of HMO utilization genes (H5-positive strains), while H5-negative strains lack an ABC-type transporter known to bind core HMO structures. H5-positive strains achieved significantly superior growth on lacto-N-tetraose and lacto-N-neotetraose. In vitro, H5-positive strains had a significant fitness advantage over H5-negative strains, which was also observed in vivo in breastfed infants. This work provides evidence of the functional implications of genetic dierences among B. infantis strains and highlights that genotype and HMO utilization phenotype should be considered when selecting a strain for probiotic use in infants

Stress-first single photon emission computed myocardial perfusion imaging

Background. Myocardial perfusion imaging (MPI) with single photon emission tomography (SPET) is widely used in coronary artery disease evaluation. Recently major dosimetric concerns have arisen. The aim of this study was to evaluate if a pre-test scoring system could predict the results of stress SPET MPI, thus avoiding two radionuclide injections. Methods. All consecutive patients (n=309) undergoing SPET MPI during the first 6 months of 2014 constituted the study group. The scoring system is based on these characteristics: age >65 years (1 point), diabetes (2 points), typical chest pain (2 points), congestive heart failure (3 points), abnormal ECG (4 points), male gender (4 points), and documented previous CAD (5 points). The patients were divided on the basis of the prediction score into 3 classes of risk for an abnormal stress-first protocol. Results. An abnormal stress SPET MPI was present in 7/31 patients (23%) with a low risk score, in 24/90 (27%) with an intermediate score risk, and in 124/188 (66%) with an high score risk. ROC curve analysis showed good prediction of abnormal stress MPI. Conclusions. Our results suggest an appropriate use of a pre-test clinical prediction formula of abnormal stress MPI in a routine clinical setting

Elevated Fecal pH Indicates a Profound Change in the Breastfed Infant Gut Microbiome Due to Reduction of \u3ci\u3eBifidobacterium\u3c/i\u3e over the Past Century

Historically, Bifidobacterium species were reported as abundant in the breastfed infant gut. However, recent studies in resource-rich countries show an increased abundance of taxa regarded as signatures of dysbiosis. It is unclear whether these differences are the product of genetics, geographic factors, or interventions such as formula feeding, antibiotics, and caesarean section. Fecal pH is strongly associated with Bifidobacterium abundance; thus, pH could be an indicator of its historical abundance. A review of 14 clinical studies published between 1926 and 2017, representing more than 312 healthy breastfed infants, demonstrated a change in fecal pH from 5.0 to 6.5 (adjusted r2 = 0.61). This trend of increasing infant fecal pH over the past century is consistent with current reported discrepancies in Bifidobacterium species abundance in the gut microbiome in resource-rich countries compared to that in historical reports. Our analysis showed that increased fecal pH and abundance of members of the families Enterobacteriaceae, Clostridiaceae, Peptostreptococcaceae, and Veillonellaceae are associated, indicating that loss of highly specialized Bifidobacterium species may result in dysbiosis, the implications of which are not yet fully elucidated. Critical assessment of interventions that restore this ecosystem, measured by key parameters such as ecosystem productivity, gut function, and long-term health, are necessary to understand the magnitude of this change in human biology over the past century