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OBJECTIVE. To test the hypothesis that an altered gut microbiota (dysbiosis) plays a role in obesity-associated osteoarthritis (OA). METHODS. Stool and blood samples were collected from 92 participants with BMI ≥ 30 kg/m(2) recruited from the Johnston County Osteoarthritis Project. OA cases (n=50) had hand plus knee OA (Kellgren-Lawrence [KL] grade ≥2 or arthroplasty). Controls (N=42) had no hand OA and KL grade 0–1 knees. Compositional analysis of stool samples was carried out by 16S rRNA amplicon sequencing. Alpha and beta diversity and differences in taxa relative abundances were determined. Blood samples were used for multiplex cytokine analysis and measures of lipopolysaccharide (LPS) and LPS binding protein. Germ-free mice were gavaged with case or control pooled fecal samples and placed on a 40% fat, high sucrose diet for 40 weeks. Knee OA was evaluated histologically. RESULTS. OA cases were slightly older with more females and higher BMI, WOMAC pain and KL grades than controls. There were no significant differences in alpha or beta diversity or genus level composition between cases and controls. Cases had higher plasma levels of osteopontin (p=0.01) and serum LPS (p

Anorexia nervosa (AN) has one of the highest mortality rates of any psychiatric disorder. Treatments are often ineffective and relapse is common. Most research attempting to understand the underlying causes and maintenance factors of AN has focused on environmental contributions, yet there is much to be explored in terms of biological risk and maintenance factors. In this paper, we focus primarily on AN research related to genetics and the complex microbial community in the gut (intestinal microbiota), and how these impact our conceptualization of this disorder. Emerging research identifying significant negative genetic correlations between AN and obesity suggests that the conditions may represent 'metabolic bookends'. The identification of underlying biological mechanisms may provide both insight into extreme weight dysregulation on both ends of the spectrum and new possible points of entry for AN treatment. Additionally, the reported microbial imbalance (dysbiosis) in the gut microbiota in AN patients, potentially due to a nutrient- and energy-deprived gut environment, implies alterations in functional and metabolic capacity of the gut microbiome. The extent to which AN and obesity can also be considered to be 'microbiome bookends' requires further investigation. Finally, we discuss ongoing and future AN projects exploring the interplay between host genomics, the environment, and cumulative microbial genomes (microbiome) as well as interventions at the microbial and gut level.

Anorexia nervosa, a severe psychiatric illness, is associated with an intestinal microbial dysbiosis. Individual microbial signatures dominate in healthy samples, even over time and under controlled conditions, but whether microbial markers of the disorder overcome inter-individual variation during the acute stage of illness or renourishment is unknown. We characterized daily changes in the intestinal microbiota in three acutely ill patients with anorexia nervosa over the entire course of hospital-based renourishment and found significant, patient-specific changes in microbial composition and diversity. This preliminary case series suggests that even in a state of pathology, individual microbial signatures persist in accounting for the majority of intestinal microbial variation. Copyright © 2017 John Wiley & Sons, Ltd and Eating Disorders Association.

Induction of mammalian heme oxygenase (HO)-1 and exposure of animals to carbon monoxide (CO) ameliorates experimental colitis. When enteric bacteria, including Escherichia coli, are exposed to low iron conditions, they express an HO-like enzyme, chuS, and metabolize heme into iron, biliverdin and CO. Given the abundance of enteric bacteria residing in the intestinal lumen, our postulate was that commensal intestinal bacteria may be a significant source of CO and those that express chuS and other Ho-like molecules suppress inflammatory immune responses through release of CO. According to real-time PCR, exposure of mice to CO results in changes in enteric bacterial composition and increases E. coli 16S and chuS DNA. Moreover, the severity of experimental colitis correlates positively with E. coli chuS expression in IL-10 deficient mice. To explore functional roles, E. coli were genetically modified to overexpress chuS or the chuS gene was deleted. Co-culture of chuS-overexpressing E. coli with bone marrow-derived macrophages resulted in less IL-12p40 and greater IL-10 secretion than in wild-type or chuS-deficient E. coli. Mice infected with chuS-overexpressing E. coli have more hepatic CO and less serum IL-12 p40 than mice infected with chuS-deficient E. coli. Thus, CO alters the composition of the commensal intestinal microbiota and expands populations of E. coli that harbor the chuS gene. These bacteria are capable of attenuating innate immune responses through expression of chuS. Bacterial HO-like molecules and bacteria-derived CO may represent novel targets for therapeutic intervention in inflammatory conditions.

Background In a recent double-blinded clinical trial the probiotic combination of L-NCFM and B-LBi07 reduced bloating symptoms in patients with functional bowel disorder; an effect more evident in those who reported abdominal pain. In mice, L-NCFM but not B-LBi07 induced colonic MOR and CB2 expression and reduced visceral sensitivity.

Anorexia nervosa (AN) continues to perplex, and new lenses with which to view the disorder are essential to advancing understanding and enhancing treatment. Although a fundamental first step in treatment, few clinical trials exist that explore how best to renourish individuals with AN, and treatment approaches typically are based on clinical opinion or guidelines.1 Moreover, gastrointestinal effects of refeeding are uncomfortable, distressing, and painful, resulting in low treatment acceptance and high dropout.

Background The intestinal microbiota has been implicated in the pathophysiology of irritable bowel syndrome (IBS). Due to the variable resolutions of techniques used to characterize the intestinal microbiota, and the heterogeneity of IBS, the defined alterations of the IBS intestinal microbiota are inconsistent. We analyzed the composition of the intestinal microbiota in a defined subgroup of IBS patients (diarrhea-predominant IBS, D-IBS) using a technique that provides the deepest characterization available for complex microbial communities. Methods Fecal DNA was isolated from 23 D-IBS patients and 23 healthy controls (HC). Variable regions V1–V3 and V6 of the 16S rRNA gene were amplified from all samples. PCR products were sequenced using 454 high throughput sequencing. The composition, diversity and richness of microbial communities were determined and compared between D-IBS and HC using the quantitative insights into microbial ecology pipeline. Key Results The contribution of bacterial groups to the composition of the intestinal microbiota differed between D-IBS and HC. D-IBS patients had significantly higher levels of Enterobacteriaceae (P = 0.03), and lower levels of Fecalibacterium genera (P = 0.04) compared to HC. β-Diversity values demonstrated significantly lower levels of UniFrac distances in HC compared to D-IBS patients. The richness of 16S rRNA sequences was significantly decreased in D-IBS patients (P