The Effects of One Anastomosis Gastric Bypass Surgery on the Gastrointestinal Tract

One anastomosis gastric bypass (OAGB) is an emerging bariatric procedure, yet data on its effect on the gastrointestinal tract are lacking. This study sought to evaluate the incidence of small-intestinal bacterial overgrowth (SIBO) following OAGB; explore its effect on nutritional, gastrointestinal, and weight outcomes; and assess post-OABG occurrence of pancreatic exocrine insufficiency (PEI) and altered gut microbiota composition. A prospective pilot cohort study of patients who underwent primary-OAGB surgery is here reported. The pre-surgical and 6-months-post-surgery measurements included anthropometrics, glucose breath-tests, biochemical tests, gastrointestinal symptoms, quality-of-life, dietary intake, and fecal sample collection. Thirty-two patients (50% females, 44.5 ± 12.3 years) participated in this study, and 29 attended the 6-month follow-up visit. The mean excess weight loss at 6 months post-OAGB was 67.8 ± 21.2%. The glucose breath-test was negative in all pre-surgery and positive in 37.0% at 6 months (p = 0.004). Positive glucose breath-test was associated with lower reported dietary intake and folate levels and higher vitamin A deficiency rates (p ≤ 0.036). Fecal elastase-1 test (FE1) was negative for all pre-surgery and positive in 26.1% at 6 months (p = 0.500). Both alpha and beta diversity decreased at 6 months post-surgery compared to pre-surgery (p ≤ 0.026). Relatively high incidences of SIBO and PEI were observed at 6 months post-OAGB, which may explain some gastrointestinal symptoms and nutritional deficiencies.

Determine independent gut microbiota-diseases association by eliminating the effects of human lifestyle factors

Lifestyle and physiological variables on human disease risk have been revealed to be mediated by gut microbiota. Low concordance between case-control studies for detecting disease-associated microbe existed due to limited sample size and population-wide bias in lifestyle and physiological variables. To infer gut microbiota-disease associations accurately, we propose to build machine learning models by including both human variables and gut microbiota. When the model’s performance with both gut microbiota and human variables is better than the model with just human variables, the independent gut microbiota -disease associations will be confirmed. By building models on the American Gut Project dataset, we found that gut microbiota showed distinct association strengths with different diseases. Adding gut microbiota into human variables enhanced the classification performance of IBD significantly; independent associations between occurrence information of gut microbiota and irritable bowel syndrome, C. difficile infection, and unhealthy status were found; adding gut microbiota showed no improvement on models’ performance for diabetes, small intestinal bacterial overgrowth, lactose intolerance, cardiovascular disease. Our results suggested that although gut microbiota was reported to be associated with many diseases, a considerable proportion of these associations may be very weak. We proposed a list of microbes as biomarkers to classify IBD and unhealthy status. Further functional investigations of these microbes will improve understanding of the molecular mechanism of human diseases.

Is it necessary to correct the intestinal microbiota disorders in chronic pancreatitis?

The frequency of intestinal microbiota disorders in patients with chronic pancreatitis (CP) is extremely high and can reach 97%. The bacterial overgrowth syndrome (SIBO) and the syndrome of increased epithelial permeability (SPEP), developing against the background of excretory insufficiency of the pancreas, affect the severity of the clinical picture of the disease, reduce the effectiveness of enzyme replacement therapy and generally contribute to the further progression of CP.The article presents a modern view on the mechanisms of the formation of SIBO and SPEP in CP. There is their aggravating effect on the course of the disease and the aggravation of disorders of the digestive and absorption processes that accompany them is shown and analyzed in the article.For decontamination of conditionally pathogenic and pathogenic flora, increasing the number and metabolic activity of indigenous microflora in patients with CP, the use of a non-absorbable broad-spectrum antibiotic rifaximin is effective. In order to restore the barrier function of the gastrointestinal mucosa, the drug of choice is rebamipid, a universal cytoprotector that affects all three levels of epithelial tissue protection (preepithelial, epithelial and subepithelial).Conclusion. CP is characterized by the complexity of its etiology and pathogenesis. Bacterial factors, in particular, SIBO and SPEP, play an essential role in the development of inflammatory changes in the pancreas. In the complex therapy of CP, it is advisable to take measures aimed at correcting disorders of the intestinal microbiota.

Diagnosis and Treatment of Irritable Bowel Syndrome: Clinical Recommendations of the Russian Gastroenterological Association and Association of Coloproctologists of Russia

Aim. Current clinical recommendations accentuate current methods for the diagnosis and treatment of irritable bowel syndrome (IBS).Key points. IBS is a functional bowel disorder manifested with recurrent, at least weekly, abdominal pain with the following attributes (any two leastwise): link to defecation, its frequency or stool shape. The symptoms are expected to persist for at minimum three months in a total six-month follow-up. Similar to other functional gastrointestinal (GI) disorders, IBS can be diagnosed basing on the patient symptoms compliance with Rome IV criteria, provided the absence of potentially symptom-causative organic GI diseases. Due to challenging differential diagnosis, IBS can be appropriately established per exclusionem, with pre-examination as follows: general and biochemical blood tests; tissue transglutaminase IgA/IgG antibody tests; thyroid hormones test; faecal occult blood test; hydrogen glucose/ lactulose breath test for bacterial overgrowth; stool test for enteric bacterial pathogens and Clostridium difficile A/B toxins; stool calprotectin test; abdominal ultrasound; OGDS, with biopsy as appropriate; colonoscopy with biopsy. The IBS sequence is typically wavelike, with alternating remissions and exacerbations often triggered by psychoemotional stress. Treatment of IBS patients includes dietary and lifestyle adjustments, various-class drug agents prescription and psychotherapeutic measures.Conclusion. Adherence to clinical recommendations can facilitate timely diagnosis and improve medical aid quality in patients with different clinical IBS variants.

Amino acid availability determines plant immune homeostasis in the rhizosphere microbiome

Microbes possess conserved microbe-associated molecular patterns (MAMPs) such as flagellin that are recognized by plant receptors to induce immunity. Despite containing the same MAMPs as pathogens, commensals thrive in the plant rhizosphere microbiome indicating they must suppress or evade host immunity. The beneficial bacteria Pseudomonas capeferrum WCS358 can suppress Arabidopsis root immunity via acidification by secreting gluconic acid. While gluconic acid is sufficient to suppress immunity, we found that it is not necessary in a second beneficial strain Pseudomonas simiae WCS417, which produces more gluconic acid than WCS358. To uncover mechanisms that contribute to the suppression of Arabidopsis immunity, we performed a forward genetic screen in EMS-mutagenized P. simiae WCS417 using a flagellin-inducible CYP71A12 pro:GUS reporter as an Arabidopsis immune readout. We identified a mutant that cannot suppress flagellin-elicited CYP71A12 pro:GUS expression or acidify the rhizosphere. Next generation sequencing revealed a mutation in the catabolic site of an ornithine carbamoyltransferase argF, which is required for arginine biosynthesis. The mutant could be complemented by expression of argF from a plasmid, and a ΔargF mutant could not suppress immunity. Fungal pathogens can use alkalization through production of ammonia and glutamate, the arginine biosynthetic precursors, to promote their own growth and virulence. Therefore, we hypothesized that the biosynthesis of specific amino acids may be necessary to reduce levels of ammonia and glutamate to prevent rhizosphere alkalization and bacterial overgrowth. Genetically blocking arginine, glutamine, or proline biosynthesis, or by adding corresponding exogenous amino acids, resulted in rhizosphere alkalization. Interestingly, exogenous amino acids caused bacterial overgrowth in a gluconic acid-deficient mutants. Our findings show that bacterial amino acid biosynthesis contributes to acidification by preventing accumulation of glutamate precursors and the resulting alkalization. Collectively this work shows that by regulating nutrient availability, plants have the potential to regulate their immune homeostasis in the rhizosphere microbiome.

New Metabolic, Digestive, and Oxidative Stress-Related Manifestations Associated with Posttraumatic Stress Disorder

Posttraumatic stress disorder (PTSD) represents a pressing and generally invalidating syndrome that is triggered by a terrifying or stressful experience, relying on recurrently reliving the traumatic event feelings associated to it, which is subsequently linked to ongoing activations of stress-related neurobiological pathways and is often associated with neurodegeneration. In this paper, we examine what lies beneath this disorder, reviewing evidence that connects PTSD with a wide array of mechanisms and its intertwined pathways that can lead to the decompensation of different pathologies, such as cardiovascular disease, gastrointestinal ailments, autoimmune disorders, and endocrine diseases. Also, the significance of the oxidative stress in this frame of reference is debated. Thus, knowing and identifying the main features of the distressing experience, the circumstances around it, as well as the neuropsychological and emotional characteristics of people prone to develop PTSD after going through disturbing incidents can offer an opportunity to anticipate the development of potential destructive consequences in several psychological dimensions: cognitive, affective, relational, behavioral, and somatic. We can also observe more closely the intricate connections of the disorder to other pathologies and their underlying mechanisms such as inflammation, oxidative stress, bacterial overgrowth syndrome, irritable bowel syndrome, metabolic disorders, oxytocin, and cortisol in order to understand it better and to optimize the course of treatment and its management. The complex foundation PTSD possesses is supported by the existing clinical, preclinical, and experimental data encompassed in the current review. Different biological systems and processes such as the hypothalamic-pituitary-adrenal axis, sympathetic nervous system, oxidative stress, inflammation, and microbiome suffer modifications and changes when it comes to PTSD; that is why targeted therapies exert tremendous alleviations of symptoms in patients diagnosed with this disorder. Therefore, this implies that PTSD is not restricted to the psychiatric domain and should be viewed as a systemic condition.

Immunoglobulin A Mucosal Immunity and Altered Respiratory Epithelium in Cystic Fibrosis

The respiratory epithelium represents the first chemical, immune, and physical barrier against inhaled noxious materials, particularly pathogens in cystic fibrosis. Local mucus thickening, altered mucociliary clearance, and reduced pH due to CFTR protein dysfunction favor bacterial overgrowth and excessive inflammation. We aimed in this review to summarize respiratory mucosal alterations within the epithelium and current knowledge on local immunity linked to immunoglobulin A in patients with cystic fibrosis.