Gastrointest. Disord., Volume 2, Issue 1 (March 2020) – 5 articles

The etiology of primary sclerosing cholangitis (PSC) is unknown. I present a case which may be indicative of a causal link between Bartonella infection and PSC. The patient presented with complaints of abdominal pain and bloody diarrhea. A colonoscopy demonstrated chronic inflammation and changes consistent with ulcerative colitis. Routine laboratory studies revealed elevated liver function tests (LFTs); ultrasound and magnetic resonance imaging (MRI) confirmed the diagnosis of PSC. Bartonella serology was positive. It is established that Bartonella infection is associated with both gastrointestinal inflammation and autoimmunity; indeed, there is an animal model for Bartonella-induced PSC. Bartonella is susceptible to treatment with vancomycin and there are case reports and small series that demonstrate that PSC responds to treatment with oral vancomycin. Because of this, it is postulated that at least some cases of PSC may be associated with Bartonella infection. The patient in this report was treated with oral vancomycin and, since then, has been in remission for both colitis and PSC. Since vancomycin is not systemically absorbed, the premise is that he suffered from Bartonella colitis and an autoimmune reaction to Bartonella causing PSC. This premise warrants further study. Full article

Background: The immune-modulator behaviour of the CCR6/CCL20 axis in multi -system pathophysiology and molecular signalling was investigated at two clinically significant time points, using a Ccr6—deficient mouse model of spontaneous colitis. Methods:Four groups of mice, (C57BL/6J, Ccr6^−/− of C57BL/6J, Winnie × Ccr6^−/− and Winnie) were utilized and (I) colonic clinical parameters (2) histology of colon, spleen, kidney and liver (3) T and B lymphocyte distribution in the spleen and MLN by flowcytometry (5) colonic CCL20, phosphorylated PI3K and phosphorylated Akt expression by immunohistochemistry and (6) colonic cytokine expression by RT-PCR were evaluated. Results: CCR6 deficiency was shown to attenuate inflammation in the spleen, liver and gut while renal histology remained unaffected. Marked focal lobular inflammation with reactive nuclear features were observed in hepatocytes and a significant neutrophil infiltration in red pulp with extra medullary hemopoiesis in the spleen existed in Winnie. These changes were considerably reduced in Winnie × Ccr6^−/− with elevated goblet cell numbers and mucus production in the colonic epithelium. Conclusions: Results indicate that Ccr6-deficiency in the colitis model contributes towards resolution of disease. Our findings demonstrate an intricate networking role for CCR6 in immune activation, which is downregulated by Ccr6 deficiency, and could provide newer clinical therapies in colitis. Full article

Introduction: Gastric electrical stimulation (GES) is a surgically implanted treatment option for drug refractory gastroparesis syndromes. Evidence supporting use of GES and the pathophysiology of gastroparesis syndromes is not widely known. We conducted a descriptive review to elucidate the pathophysiology of gastroparesis syndromes, with particular focus on gastrointestinal neuromodulation and the known mechanisms of action of GES. Methods: A descriptive review of PubMed, Web of Science and Cochrane Library was conducted using the keywords gastric electrical stimulation, gastroparesis, nausea, vomiting, neuromodulation, gastroparesis syndromes, central nervous system, gastric pacing and electrical stimulation. Results: 1040 potentially relevant articles were identified, of which 34 were included. These studies explored various central and peripheral effects of GES, as well as its effect on quality of life, hospital stay, mortality and health-related costs. Conclusion: Although evidence supporting gastrointestinal (GI) electrical stimulation and GI neuromodulation use is not widely known, GES does seem to offer significant improvement in symptom control, quality of life and other effects to many patients. GES exerts its effects through multiple central and peripheral mechanisms and has potential to modify the natural history of disease. Future work on gastroparetic syndromes and their treatment might be better focused in terms of pathophysiologic mechanisms. Improving outcomes with specific neuromodulation therapies, like GES, may offer improvements in health for many patients with refractory upper gastrointestinal symptoms. Full article

Across the world there is an increasingly heavy burden of noncommunicable diseases related to obesity, mental health, and atopic disease. In a previous publication, we followed the developing idea that that these conditions arise as our microbiome loses diversity, but there seems to be no generally applicable way to assess the significance of this loss. Our work revisited the findings of the African studies by Denis Burkitt who reported that the frequency of what he called Western diseases were inversely proportional to the average faecal volumes of affected populations. Although he ascribed this to fibre in the diet, it now seems more likely that the drop in faecal volume with the onset of disease is due to the loss of a fully functioning microbiome. We suggested that the microbiome could be considered to be a single mutualistic microbial community interacting with our body by two complementary sets of semiochemicals, i.e., allomones to feed the microbiota by facilitating the efficient transfer of nutrition through the gut and kairomones to calibrate our immune system by an as yet unknown mechanism. The bioactive compounds, dopamine and serotonin, are known to be present in the gut lumen under the influence of intestinal microbiota and we suggest that these are part of this allomone-like system. In light of this possibility, it is of critical importance to develop a method of quantifying the microbiome effectiveness. Ingestible sensors consist of a miniaturized detector and transmitter packed into a capsule that is swallowed and tracked through the intestine. The aim of this article is to explore the possible development of such ingestible detectors for these or other compounds that can act as a surrogate marker for microbiome effectiveness. We consider that the ability to provide real-time quantitative information on the interaction of the microbiome with different nutrients promises to be a valuable new tool to unravel the mystery of these noncommunicable illnesses, i.e., microbiome-function deficiency diseases. Full article