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Diabetes and cardiovascular disease (CVD) have evolved as the leading cause of mortality and morbidity worldwide. In addition to traditional risk factors, recent studies have established that the human microbiota, particularly gut bacteria, plays a role in the development of diabetes and CVD. Although the presence of microbes in blood has been known for centuries, mounting evidence in this metagenomic era provides new insights into the role of the blood microbiota in the pathogenesis of non-infectious diseases such as diabetes and CVD. We highlight the origin and physiology of the blood microbiota and circulating microbial metabolites in relation to the etiology and progression of diabetes and CVD. We also discuss translational perspectives targeting the blood microbiota in the diagnosis and treatment of diabetes and CVD.

Impaired colon motility is one of the leading problems associated with inflammatory bowel disease (IBD). An expanding body of evidence supports the role of microbiome in normal gut function and in progression of IBD. The objective of this work is to determine whether diseased full thickness colon specimens, including the neuromuscular region (critical for colon motility function), contain specific oral and gut pathogens. In addition, we compared the differences in colon microbiome between Caucasians (CA) and African Americans (AA). Thirty-nine human full thickness colon (diseased colon and adjacent healthy colon) specimens were collected from Crohn's Colitis (CC) or Ulcerative Colitis (UC) patients while they underwent elective colon surgeries. We isolated and analyzed bacterial ribosomal RNA (rRNA) from colon specimens by amplicon sequencing of the 16S rRNA gene region. The microbiome proportions were quantified into Operational Taxonomic Units (OTUs) by analysis with Quantitative Insights Into Microbial ecology (QIIME) platform. Two hundred twenty-eight different bacterial species were identified by QIIME analysis. However, we could only decipher the species name of fifty-three bacteria. Our results show that proportion of non-detrimental bacteria in CC or UC colon samples were altered compared to adjacent healthy colon specimens. We further show, for the first time in full thickness colon specimens, that microbiome of CC and UC diseased specimens is dominated by putative oral pathogens belonging to the Phyla Firmicutes (Streptococcus, Staphylococcus, Peptostreptococcus), and Fusobacteria (Fusobacterium). In addition, we have identified patterns of differences in microbiome levels between CA and AA specimens with potential implications for health disparities research. Overall, our results suggest a significant association between oral and gut microbes in the modulation of colon motility in colitis patients.

Background Organophosphates are the most frequently and largely applied insecticide in the world due to their biodegradable nature. Gut microbes were shown to degrade organophosphates and cause intestinal dysfunction. The diabetogenic nature of organophosphates was recently reported but the underlying molecular mechanism is unclear. We aimed to understand the role of gut microbiota in organophosphate-induced hyperglycemia and to unravel the molecular mechanism behind this process. Results Here we demonstrate a high prevalence of diabetes among people directly exposed to organophosphates in rural India (n = 3080). Correlation and linear regression analysis reveal a strong association between plasma organophosphate residues and HbA1c but no association with acetylcholine esterase was noticed. Chronic treatment of mice with organophosphate for 180 days confirms the induction of glucose intolerance with no significant change in acetylcholine esterase. Further fecal transplantation and culture transplantation experiments confirm the involvement of gut microbiota in organophosphate-induced glucose intolerance. Intestinal metatranscriptomic and host metabolomic analyses reveal that gut microbial organophosphate degradation produces short chain fatty acids like acetic acid, which induces gluconeogenesis and thereby accounts for glucose intolerance. Plasma organophosphate residues are positively correlated with fecal esterase activity and acetate level of human diabetes. Conclusion Collectively, our results implicate gluconeogenesis as the key mechanism behind organophosphate-induced hyperglycemia, mediated by the organophosphate-degrading potential of gut microbiota. This study reveals the gut microbiome-mediated diabetogenic nature of organophosphates and hence that the usage of these insecticides should be reconsidered. Electronic supplementary material The online version of this article (doi:10.1186/s13059-016-1134-6) contains supplementary material, which is available to authorized users.

An extract from the seeds of Trigonella foenum graecum (Fenugreek) was evaluated for its protective effect against hydrogen peroxide (H2O2) induced oxidation in normal sheep erythrocytes (red blood cells (RBCs)). RBCs, treated with increasing concentrations of 30% H2O2 along with fenugreek seed extract (FSE) were analyzed for hemolysis and lipid peroxidation. Sheep RBCs treated with increasing concentrations of glucose, to study effect of high glucose level or hyperglycemia on normal SRBC, were found to be more susceptible to lipid peroxidation than those from normal subjects. However, on treatment with FSE, the oxidative modifications in both the groups (RBCs treated with glucose and not treated with glucose) were found to reduce significantly. The inhibition of lipid peroxidation was concentration-dependent up to 100 μl of extract, which contained 0.75 mM gallic acid equivalent (GAE) of phenolic compounds. The total phenolic content in the extract was determined spectrophotometrically according to the Folin-Ciocalteau procedure and was expressed as mg or mM GAE. The results indicate that the extract of fenugreek seeds contains antioxidants and protects cellular structures from oxidative damage. These findings demonstrate the potent antioxidant properties of the fenugreek seeds. Key words: Fenugreek seed extract (FSE), type II diabetes, osmofragility test, lipid peroxidation.

Brucella spp. are facultative intracellular pathogens that cause brucellosis in various mammals including humans. Brucella survive inside the host cells by forming vacuoles and subverting host defence systems. This study was aimed to predict the secretion systems and the secretomes of Brucella spp. from 39 complete genome sequences available in the databases. Furthermore, an attempt was made to identify the type IV secretion effectors and their interactions with host proteins. We predicted the secretion systems of Brucella by the KEGG pathway and SecReT4. Brucella secretomes and type IV effectors (T4SEs) were predicted through genome-wide screening using JVirGel and S4TE, respectively. Protein–protein interactions of Brucella T4SEs with their hosts were analyzed by HPIDB 2.0. Genes coding for Sec and Tat pathways of secretion and type I (T1SS), type IV (T4SS) and type V (T5SS) secretion systems were identified and they are conserved in all the species of Brucella. In addition to the well-known VirB operon coding for the type IV secretion system (T4SS), we have identified the presence of additional genes showing homology with T4SS of other organisms. On the whole, 10.26 to 14.94% of total proteomes were found to be either secreted (secretome) or membrane associated (membrane proteome). Approximately, 1.7 to 3.0% of total proteomes were identified as type IV secretion effectors (T4SEs). Prediction of protein–protein interactions showed 29 and 36 host–pathogen specific interactions between Bos taurus (cattle)–B. abortus and Ovis aries (sheep)–B. melitensis, respectively. Functional characterization of the predicted T4SEs and their interactions with their respective hosts may reveal the secrets of host specificity of Brucella.

We have isolated a Staphylococcus arlettae strain, strain CVD059, from the blood of a rheumatic mitral stenosis patient. Here, we report the genome sequence and potential virulence factors of this clinical isolate. The draft genome of S. arlettae CVD059 is 2,565,675 bp long with a G+C content of 33.5%.

Cardiovascular diseases (CVDs) have a complex aetiology determined by risk factors, which include genetic and environmental factors. Chronic infection and inflammation is reported to be a pathogenic determinant for the development of CVDs. Here, we report the prevalence of bacterial pathogens in the circulation of CVD patients in Madurai, India. Blood culturing was performed using BD BACTEC automated culture system and organisms were identified by16S rRNA gene sequence analysis. From a total of 133 samples screened, 47 samples showed culture positive which indicates a high level of bacteraemia in CVD patients. From the 47 samples that showed growth, we have identified 57 bacterial isolates comprising 35 different species. Coagulase negative Staphylococci (CoNS) was the most predominant group of bacteria and other notable bacterial species isolated in this study are discussed.