The Role of Antibiotics in Gut Microbiota Modulation: The Eubiotic Effects of Rifaximin

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Abstract

Antibiotics are mainly used in clinical practice for their activity against pathogens, but they also alter the composition of commensal gut microbial community. Rifaximin is a non-absorbable antibiotic with additional effects on the gut microbiota about which very little is known. It is still not clear to what extent rifaximin can be able to modulate gut microbiota composition and diversity in different clinical settings. Studies based on culture-dependent techniques revealed that rifaximin treatment promotes the growth of beneficial bacteria, such as Bifidobacteria and Lactobacilli. Accordingly, our metagenomic analysis carried out on patients with different gastrointestinal and liver diseases highlighted a significant increase in Lactobacilli after rifaximin treatment, persisting in the short time period. This result was independent of the disease background and was not accompanied by a significant alteration of the overall gut microbial ecology. This suggests that rifaximin can exert important eubiotic effects independently of the original disease, producing a favorable gut microbiota perturbation without changing its overall composition and diversity.

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Differences between tissue-associated intestinal microfloras of patients with Crohn's disease and ulcerative colitis.

Uri Gophna, Katrin Sommerfeld, Sharon Gophna … (2006)

A leading hypothesis for the role of bacteria in inflammatory bowel diseases is that an imbalance in normal gut flora is a prerequisite for inflammation. Testing this hypothesis requires comparisons between the microbiota compositions of ulcerative colitis and Crohn's disease patients and those of healthy individuals. In this study, we obtained biopsy samples from patients with Crohn's disease and ulcerative colitis and from healthy controls. Bacterial DNA was extracted from the tissue samples, amplified using universal bacterial 16S rRNA gene primers, and cloned into a plasmid vector. Insert-containing colonies were picked for high-throughput sequencing, and sequence data were analyzed, yielding species-level phylogenetic data. The clone libraries yielded 3,305 sequenced clones, representing 151 operational taxonomical units. There was no significant difference between floras from inflamed and healthy tissues from within the same individual. Proteobacteria were significantly (P = 0.0007) increased in Crohn's disease patients, as were Bacteroidetes (P < 0.0001), while Clostridia were decreased in that group (P < 0.0001) in comparison with the healthy and ulcerative colitis groups, which displayed no significant differences. Thus, the bacterial flora composition of Crohn's patients appears to be significantly altered from that of healthy controls, unlike that of ulcerative colitis patients. Imbalance in flora in Crohn's disease is probably not sufficient to cause inflammation, since microbiotas from inflamed and noninflamed tissues were of similar compositions within the same individual.

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Transient inability to manage proteobacteria promotes chronic gut inflammation in TLR5-deficient mice.

Frederic A Carvalho, Omry Koren, Julia K Goodrich … (2012)

Colitis results from breakdown of homeostasis between intestinal microbiota and the mucosal immune system, with both environmental and genetic influencing factors. Flagellin receptor TLR5-deficient mice (T5KO) display elevated intestinal proinflammatory gene expression and colitis with incomplete penetrance, providing a genetically sensitized system to study the contribution of microbiota to driving colitis. Both colitic and noncolitic T5KO exhibited transiently unstable microbiotas, with lasting differences in colitic T5KO, while their noncolitic siblings stabilized their microbiotas to resemble wild-type mice. Transient high levels of proteobacteria, especially enterobacteria species including E. coli, observed in close proximity to the gut epithelium were a striking feature of colitic microbiota. A Crohn's disease-associated E. coli strain induced chronic colitis in T5KO, which persisted well after the exogenously introduced bacterial species had been eliminated. Thus, an innate immune deficiency can result in unstable gut microbiota associated with low-grade inflammation, and harboring proteobacteria can drive and/or instigate chronic colitis. Copyright © 2012 Elsevier Inc. All rights reserved.

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Innate and adaptive immunity interact to quench microbiome flagellar motility in the gut.

Largus Angenent, Teresa M. Bell, J. S. Werner … (2013)

Gut mucosal barrier breakdown and inflammation have been associated with high levels of flagellin, the principal bacterial flagellar protein. Although several gut commensals can produce flagella, flagellin levels are low in the healthy gut, suggesting the existence of control mechanisms. We find that mice lacking the flagellin receptor Toll-like receptor 5 (TLR5) exhibit a profound loss of flagellin-specific immunoglobulins (Igs) despite higher total Ig levels in the gut. Ribotyping of IgA-coated cecal microbiota showed Proteobacteria evading antibody coating in the TLR5(-/-) gut. A diversity of microbiome members overexpressed flagellar genes in the TLR5(-/-) host. Proteobacteria and Firmicutes penetrated small intestinal villi, and flagellated bacteria breached the colonic mucosal barrier. In vitro, flagellin-specific Ig inhibited bacterial motility and downregulated flagellar gene expression. Thus, innate-immunity-directed development of flagellin-specific adaptive immune responses can modulate the microbiome's production of flagella in a three-way interaction that helps to maintain mucosal barrier integrity and homeostasis. Copyright © 2013 Elsevier Inc. All rights reserved.

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Journal

Journal ID (publisher-id): DDI

Journal ID (nlm-ta): Dig Dis

Journal ID (doi): 10.1159/issn.0257-2753

Title: Digestive Diseases

Publisher: S. Karger AG

ISBN: 978-3-318-05835-2

ISBN: 978-3-318-05836-9

ISSN (Print): 0257-2753

ISSN (Electronic): 1421-9875

Publication date Subscription-year: 2016

Publication date (Print): March 2016

Publication date (Electronic): 30 March 2016

Volume: 34

Issue: 3

Pages: 269-278

Affiliations

^aInternal Medicine and Gastroenterology Division and ^bInstitute of Microbiology, A. Gemelli Hospital, Rome, Italy

Author notes

*Dr. Francesca Romana Ponziani, MD, Internal Medicine and Gastroenterology Division, A. Gemelli Hospital, Largo A. Gemelli 8, IT-00168, Rome (Italy), E-Mail francesca.ponziani@yahoo.it

Article

Publisher ID: 443361 Other ID: Dig Dis 2016;34:269-278

DOI: 10.1159/000443361

PubMed ID: 27027301

SO-VID: b6fe5ec6-c4e2-4808-9c29-ea6d7e5f2313

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Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

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Figures: 5, Tables: 2, References: 49, Pages: 10

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The Role of Antibiotics in Gut Microbiota Modulation: The Eubiotic Effects of Rifaximin

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Abstract

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Karger: Gastroenterology

Most cited references 34

Differences between tissue-associated intestinal microfloras of patients with Crohn's disease and ulcerative colitis.

Transient inability to manage proteobacteria promotes chronic gut inflammation in TLR5-deficient mice.

Innate and adaptive immunity interact to quench microbiome flagellar motility in the gut.

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