http://www.umassmed.edu/globalassets/immunology-and-microbiology/documents/papers-for-bbs821-2015/nov-24-reviewfor-general-info.pdf

Role of the Microbiota in Immunity and Inflammation

http://microbecol.khu.ac.kr/PDF_paper/TiB2015.pdf

Proteobacteria: Microbial signature of dysbiosis in gut microbiota

In recent years, several associations between common chronic human disorders and altered gut microbiome composition and function have been reported. In most of these reports, treatment regimens were not controlled for and conclusions could thus be confounded by the effects of various drugs on the microbiota, which may obscure microbial causes, protective factors or diagnostically relevant signals. Our study addresses disease and drug signatures in the human gut microbiome of type 2 diabetes mellitus (T2D). Two previous quantitative gut metagenomics studies of T2D patients that were unstratified for treatment yielded divergent conclusions regarding its associated gut microbial dysbiosis. Here we show, using 784 available human gut metagenomes, how antidiabetic medication confounds these results, and analyse in detail the effects of the most widely used antidiabetic drug metformin. We provide support for microbial mediation of the therapeutic effects of metformin through short-chain fatty acid production, as well as for potential microbiota-mediated mechanisms behind known intestinal adverse effects in the form of a relative increase in abundance of Escherichia species. Controlling for metformin treatment, we report a unified signature of gut microbiome shifts in T2D with a depletion of butyrate-producing taxa. These in turn cause functional microbiome shifts, in part alleviated by metformin-induced changes. Overall, the present study emphasizes the need to disentangle gut microbiota signatures of specific human diseases from those of medication.

/pdf/disentangling-type-2-diabetes-and-metformin-treatment-21j3g0gq6a.pdf

Disentangling type 2 diabetes and metformin treatment signatures in the human gut microbiota

Rheumatoid arthritis (RA) is a prevalent systemic autoimmune disease, caused by a combination of genetic and environmental factors. Animal models suggest a role for intestinal bacteria in supporting the systemic immune response required for joint inflammation. Here we performed 16S sequencing on 114 stool samples from rheumatoid arthritis patients and controls, and shotgun sequencing on a subset of 44 such samples. We identified the presence of Prevotella copri as strongly correlated with disease in new-onset untreated rheumatoid arthritis (NORA) patients. Increases in Prevotella abundance correlated with a reduction in Bacteroides and a loss of reportedly beneficial microbes in NORA subjects. We also identified unique Prevotella genes that correlated with disease. Further, colonization of mice revealed the ability of P. copri to dominate the intestinal microbiota and resulted in an increased sensitivity to chemically induced colitis. This work identifies a potential role for P. copri in the pathogenesis of RA.

/pdf/expansion-of-intestinal-prevotella-copri-correlates-with-1q9uc6fis7.pdf

Expansion of intestinal Prevotella copri correlates with enhanced susceptibility to arthritis

A dense resident microbial community in the gut, referred as the commensal microbiota, coevolved with the host and is essential for many host physiological processes that include enhancement of the intestinal epithelial barrier, development of the immune system and acquisition of nutrients. A major function of the microbiota is protection against colonization by pathogens and overgrowth of indigenous pathobionts that can result from the disruption of the healthy microbial community. The mechanisms that regulate the ability of the microbiota to restrain pathogen growth are complex and include competitive metabolic interactions, localization to intestinal niches and induction of host immune responses. Pathogens, in turn, have evolved strategies to escape from commensal-mediated resistance to colonization. Thus, the interplay between commensals and pathogens or indigenous pathobionts is critical for controlling infection and disease. Understanding pathogen-commensal interactions may lead to new therapeutic approaches to treating infectious diseases.

/pdf/control-of-pathogens-and-pathobionts-by-the-gut-microbiota-3svxys7jbk.pdf

Control of pathogens and pathobionts by the gut microbiota.

Supplementary Materials for Host-Derived Nitrate Boosts Growth of E. coli in the Inflamed Gut

Salmonella enteritidis epidemic [2] (multiple letters)

Required for Enteritis in Calves -Induced Cell Death Is Not Salmonella

serovarTyphimurium,causealocalizedgastroenteritisinimmunocompetent individuals, which is characterized by acuteintestinal inﬂammation and diarrhea (reviewed in references 2and 3). The importance of innate immune responses during gas-troenteritisisillustratedbytherapidonsetofintestinalinﬂamma-tion, which gives rise to symptoms within 24 h of ingesting

Renée M. Tsolis

Papers

Supplementary Materials for Host-Derived Nitrate Boosts Growth of E. coli in the Inflamed Gut

Salmonella enteritidis epidemic [2] (multiple letters)

Required for Enteritis in Calves -Induced Cell Death Is Not Salmonella

Serovar Typhimurium Colitis enterica Interferon during Acute Salmonella Neutrophils Are a Source of Gamma