Re: Levine et al. Fecal Hydrogen Sulfide Production in Ulcerative Colitis

Florin, Timothy H.; Khalil, Dalia; Lenarczyck, A.; Moody, Steven B.; Cowley, David

doi:10.1111/j.1572-0241.1998.02638.x

Cited by 3 publications

(2 citation statements)

References 7 publications

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“…These changes do not happen in ileostomies before IPAA,100, 101 and also are more prominent in pouches from UC patients compared with FAP patients, 95 arguing that fecal stasis may be a contributing factor in the metaplasia process. Sulfomucin provides a metabolic substrate for sulfate-reducing bacteria such as Bacteroides fragilis ,102, 103, 104 which promote colonization and expansion of these bacteria, and explains the high prevalence of sulfate-reducing bacteria in UC, compared with minimal or no colonization in FAP pouches 95, 96, 105. What has yet to be well characterized are the microbiota differences between UC and FAP ileostomies, before IPAA occurs, which may help elucidate why metaplasia and pouchitis occur to a greater extent in UC patients.…”

Section: Disease Models Of Dysbiosis In the Small Intestinementioning

confidence: 99%

The Structure and Function of the Human Small Intestinal Microbiota: Current Understanding and Future Directions

Kastl

Terry

et al. 2020

Cellular and Molecular Gastroenterology and Hepatology

253

172

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There is limited information about the small intestinal microbiota, an ecosystem that is relevant to many physiologic mechanisms and pathologic states. Here, we highlight human and animal studies to advance understanding of microbe-influenced human conditions, and the fundamental distinctions of this population relative to the large intestine. Despite growing literature characterizing the fecal microbiome and its association with health and disease, few studies have analyzed the microbiome of the small intestine. Here, we examine what is known about the human small intestinal microbiota in terms of community structure and functional properties. We examine temporal dynamics of select bacterial populations in the small intestine, and the effects of dietary carbohydrates and fats on shaping these populations. We then evaluate dysbiosis in the small intestine in several human disease models, including small intestinal bacterial overgrowth, short-bowel syndrome, pouchitis, environmental enteric dysfunction, and irritable bowel syndrome. What is clear is that the bacterial biology, and mechanisms of bacteria-induced pathophysiology, are enormously broad and elegant in the small intestine. Studying the small intestinal microbiota is challenged by rapidly fluctuating environmental conditions in these intestinal segments, as well as the complexity of sample collection and bioinformatic analysis. Because the functionality of the digestive tract is determined primarily by the small intestine, efforts must be made to better characterize this unique and important microbial ecosystem.

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Section: Disease Models Of Dysbiosis In the Small Intestinementioning

confidence: 99%

The Structure and Function of the Human Small Intestinal Microbiota: Current Understanding and Future Directions

Kastl

Terry

et al. 2020

Cellular and Molecular Gastroenterology and Hepatology

253

172

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“…6,7 Additionally, pathogenic sulfur-reducing, bile-tolerant bacteria, which produce toxic and proinammatory hydrogen sulde and exacerbate intestinal inammation, are increased in the gut of UC patients. 8,9 Besides bacteria, intestinal fungi also exhibit a signicant change during inammatory conditions. Denaturing gradient gel electrophoresis analysis of fungal 18S rDNA showed different fungal proles between UC patients and healthy individuals, and an increased proportion of Candida albicans was found in the colons of CD patients, 10,11 causing aggravated mucosal injury and generation of anti-Saccharomyces cerevisiae antibodies (ASCA).…”

Section: Introductionmentioning

confidence: 99%

Fungal–bacterial interactions in mice with dextran sulfate sodium (DSS)-induced acute and chronic colitis

Qiu

et al. 2016

RSC Adv.

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The commensal intestinal microbiota plays critical roles in the initiation and development of inflammatory bowel diseases (IBD). However, the importance of intestinal fungi and their interactions with bacteria in the pathogenesis of IBD is unclear. In this study, anti-fungal drugs (fluconazole or Amphotericin B [AmpB]) were administered to control mice and those treated, acutely (A-DSS) and chronically (C-DSS) with DSS. The severity of colonic inflammation was assessed, and pro-inflammatory cytokine levels in the colonic mucosa and serum were detected by real-time PCR and multiplex ELISA assay, respectively. The colonic bacterial 16S rDNA V3 region was analysed in normal and anti-fungal drug-treated mice by pyrosequencing. Specific bacterial genera related to IBD, butyryl-CoA/acetate-CoA transferase (a key transferase for butyrate production in bacteria) and tight-junction proteins (occludin and ZO-1) in the colonic mucosa were detected by real-time PCR and/or western blot. The results showed that compared with controls，intestinal Bacteroides, Alistipes, and Lactobacillus were increased in fluconazole treated mice; while only Alistipes was increased in AmpB treated mice. Clostridium cluster XIVa and butyryl-CoA/acetate-CoA transferase levels were reduced in both groups. Treatment with a high dose of anti-fungal drugs dampened colonic occludin and ZO-1, aggravated A-DSS colitis, and exhibited no beneficial role in C-DSS colitis. However, reducing fluconazole concentration to an appropriate dose attenuated C-DSS colitis. In conclusion, fungi are important co-operators with bacteria in maintaining intestinal micro-ecological equilibrium. Extensive clearance of gut fungi could disrupt intestinal bacterial homeostasis and have an adverse impact on IBD. Studies investigating the intestinal fungal-bacterial interactions would aid the appropriate use of anti-fungal drugs in treating IBD. BACKGROUND Inflammatory bowel diseases (IBDs) such as ulcerative colitis (UC) and Crohn's disease (CD), are caused by multiple factors, including genetics, environment, immune dysfunction, and disturbance of the intestinal microbiota. The latter comprises a large and diverse community of bacteria, fungi, viruses, and archaea 1 . The intestinal microbiota plays vital roles in developing and maintaining host immunology, physiology, nutrition, and metabolism 2 . Patients with IBD are usually characterised by disturbances in their intestinal microflora. Several studies have reported an increased abundance of Gammaproteobacteria and Enterobacteriaceae, and decreased abundance of Firmicutes in both UC and CD patients 3-5 . Numbers of bacteria producing butyrate, an important short chain fatty acid (SCFA) that plays a major role in promoting visceral function and integrity, are significantly decreased in the gut of IBD patients 6, 7 .Additionally, pathogenic sulfur-reducing, bile-tolerant bacteria, which produce toxic and proinflammatory hydrogen sulfide and exacerbate intestinal inflammation, are increased in the gut of UC patients 8, 9 . Besi...

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Pathogenesis of and Unifying Hypothesis for Idiopathic Pouchitis

Coffey

Rowan²,

Burke³

et al. 2009

Am J Gastroenterol

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Ileal pouch-anal anastomosis is the procedure of choice in the surgical management of refractory ulcerative colitis. Pouchitis affects up to 60% of patients following ileal pouch-anal anastomosis for ulcerative colitis. It overlaps significantly with ulcerative colitis such that improvements in our understanding of one will impact considerably on the other. The symptoms are distressing and impinge significantly on patients' quality of life. Despite 30 years of scientific and clinical investigation, the pathogenesis of pouchitis is unknown; however, recent advances in molecular and cell biology make a synergistic hypothesis possible. This hypothesis links interaction between epithelial metaplasia, changes in luminal bacteria (in particular sulfate-reducing bacteria), and altered mucosal immunity. Specifically, colonic metaplasia supports colonization by sulfate-reducing bacteria that produce hydrogen sulfide. This causes mucosal depletion and subsequent inflammation. Although in most cases antibiotics lead to bacterial clearance and symptom resolution, immunogenetic subpopulations can develop a chronic refractory variant of pouchitis. The aims of this paper are to discuss proposed pathogenic mechanisms and to describe a novel mechanism that combines many hypotheses and explains several aspects of pouchitis. The implications for the management of both pouchitis and ulcerative colitis are discussed.

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Re: Levine et al. Fecal Hydrogen Sulfide Production in Ulcerative Colitis

Cited by 3 publications

References 7 publications

The Structure and Function of the Human Small Intestinal Microbiota: Current Understanding and Future Directions

The Structure and Function of the Human Small Intestinal Microbiota: Current Understanding and Future Directions

Fungal–bacterial interactions in mice with dextran sulfate sodium (DSS)-induced acute and chronic colitis

Pathogenesis of and Unifying Hypothesis for Idiopathic Pouchitis

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