Isolation and gut microbiota modulation of antibiotic-resistant probiotics from human feces

Tian, Peng; Xu, Bo; Sun, Han; Li, Xiuying; Li, Zhi; Wei, Pijin

doi:10.1016/j.diagmicrobio.2014.04.002

Cited by 7 publications

(6 citation statements)

References 45 publications

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“…A multitude of extrinsic factors could be listed that can have a major influence on changes in the intestinal microbiota but one of the most important etiological factors involved is the use of antibiotics, with important changes in intestinal microbiota seen following their use [26,27]. Several studies have explored this field in both animals and humans, concurring on changes in the intestinal microbiota over a period of time, with their subsequent re-establishment [27,28], while others have described persistent effects with a long-term impact on the microbiota, where recovery may sometimes be incomplete [29,30,31], causing rapid and significant reductions in taxonomic richness, diversity, and uniformity [29,32]. In agreement with the literature [26,31,33,34], we observed early secondary changes in biodiversity after conventional antibiotic therapy [32,34].…”

Section: Discussionmentioning

confidence: 99%

H. pylori Eradication Treatment Alters Gut Microbiota and GLP-1 Secretion in Humans

Cornejo‐Pareja

Martín‐Núñez

Roca-Rodríguez

et al. 2019

JCM

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Changes in the intestinal microbial community and some metabolic disturbances, including obesity and type2 diabetes, are related. Glucagon-like peptide-1 (GLP-1) regulates glucose homeostasis. Microbiota have been linked to incretin secretion. Antibiotic use causes changes in microbial diversity and composition. Our aim was to evaluate the relationship between microbiota changes and GLP-1 secretion. A prospective case-control study with a Helicobacter pylori-positive patient model involving subjects under eradication therapy (omeprazole, clarithromycin, and amoxicillin). Forty patients with H. pylori infection and 20 matched participants, but negative for H. pylori antigen. Patients were evaluated before and two months after treatment. We analyzed anthropometric measurements, carbohydrate metabolism, lipid profile, and C-reactive protein. Gut microbiota composition was analyzed through 16S rRNA amplicon sequencing (IlluminaMiSeq). Eradication treatment for H. pylori decreased bacterial richness (Chao1, p = 0.041). Changes in gut microbiota profiles were observed at phylum, family, genus and species levels. GLP-1 secretion and variables of carbohydrate metabolism were improved. Correlations were seen between GLP-1 changes and variations within microbial community abundances, specifically Bifidobacterium adolescentis, the Lachnobacterium genus, and Coriobacteriaceae family. A conventional treatment to eradicate H. pylori could improve carbohydrate metabolism possibly in relation with an increase in GLP-1 secretion. GLP-1 secretion may be related to alterations in intestinal microbiota, specifically Lachnobacterium, B. adolescentis and Coriobacteriaceae.

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Section: Discussionmentioning

confidence: 99%

H. pylori Eradication Treatment Alters Gut Microbiota and GLP-1 Secretion in Humans

Cornejo‐Pareja

Martín‐Núñez

Roca-Rodríguez

et al. 2019

JCM

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“…Conflicting positions have been taken regarding the benefits versus risk of inclusion of antibiotic‐resistant bacterial strains in probiotics . Antibiotic‐resistant bacteria might improve protection against AAGS, but they also could serve as a source of antibiotic‐resistant genes for normal flora . As a result, the use of resistant strains in probiotics generally is discouraged, and it is explicitly banned by the European Food Safety Authority .…”

Section: Discussionmentioning

confidence: 99%

Randomized, Controlled, Crossover trial of Prevention of Clindamycin‐Induced Gastrointestinal Signs Using a Synbiotic in Healthy Research Cats

Stokes

Price

Whittemore

2017

Veterinary Internal Medicne

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BackgroundSynbiotics often are prescribed to limit antibiotic‐associated gastrointestinal signs (AAGS) in cats, but data to support this recommendation are lacking.ObjectiveTo determine whether synbiotic co‐administration mitigates AAGS in healthy research cats treated with clindamycin.Animals16 healthy research cats.MethodsA randomized, double‐blinded, placebo‐controlled, 2‐way, 2‐period, crossover study with a 6‐week washout was performed. Each study period consisted of a 1‐week baseline and a 3‐week treatment period. Cats received 75 mg clindamycin with food once daily for 3 weeks, followed 1 hour later by either 2 capsules of a synbiotic or placebo. Food consumption, vomiting, fecal score, and completion of treatment were compared using repeated measures split plot or crossover designs with covariates, with P < 0.05 considered significant.ResultsCats that received the synbiotic were more likely to complete treatment in period 1 (100% vs. 50%, P = 0.04). Cats vomited less when receiving the synbiotic but this was not significant, but there were significant period effects (F‐value = 11.4, P < 0.01). Cats had higher food intake while receiving the synbiotic (F‐value = 31.1, P < 0.01) despite period effects (F‐value = 8.6, P < 0.01). There was no significant effect of treatment on fecal scores, which significantly increased over time (F‐value = 17.9, P < 0.01).Conclusions and Clinical ImportanceAdministration of a synbiotic 1 hour after clindamycin administration decreased hyporexia and vomiting in healthy cats. Additionally, significant period effects suggest that clinical benefits of synbiotic administration persist for at least 6 weeks after discontinuation, decreasing the severity of AAGS in cats that subsequently received clindamycin with placebo. Unlike in people, synbiotic administration did not decrease antibiotic‐associated diarrhea.

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“…The AAD model was induced by gavage daily with 2 ml of normal saline containing a mixture of clindamycin (Hisoar Pharmaceutical, Zhejiang, China), ampicillin (Jianmin Pharmaceutical Group Co., Ltd., Wuhan, China), and streptomycin (Lukang Pharmaceutical Co., Shandong, China) at various doses: low dose (combination of 25 mg/ml clindamycin, 27.75 mg/ml ampicillin, and 13.88 mg/ml streptomycin); middle dose (combination of 50 mg/ml clindamycin, 55.5 mg/ml ampicillin, and 27.75 mg/ml streptomycin); high dose (combination of 75 mg/ml clindamycin, 83.25 mg/ml ampicillin, and 41.63 mg/ml streptomycin). The antibiotics were gavaged for 7 days, and the doses were determined to be 1.35, 2.70, and 4.05 times the maximum human equivalent dose, respectively, based on previous studies ( 20 , 21 ). Weight, water intake, and the presence of diarrhea were measured every second day during the experimental period.…”

Section: Methodsmentioning

confidence: 99%

Bacteroides fragilis Protects Against Antibiotic-Associated Diarrhea in Rats by Modulating Intestinal Defenses

Zhang

Zhu

et al. 2018

Front. Immunol.

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Antibiotic-associated diarrhea (AAD) is iatrogenic diarrhea characterized by disruption of the gut microbiota. Probiotics are routinely used to treat AAD in clinical practice; however, the effectiveness and mechanisms by which probiotics alleviate symptoms remain poorly understood. We previously isolated a non-toxic Bacteroides fragilis strain ZY-312, which has been verified to be beneficial in certain infection disorders. However, the precise role of this commensal bacterium in AAD is unknown. In this study, we successfully established an AAD rat model by exposing rats to appropriate antibiotics. These rats developed diarrhea symptoms and showed alterations in their intestinal microbiota, including overgrowth of some pathogenic bacteria. In addition, gastrointestinal barrier defects, indicated by compromised aquaporin expression, aberrant tight junction proteins, and decreased abundance of mucus-filled goblet cells, were also detected in ADD rats compared with control animals. Of note, oral treatment with B. fragilis strain ZY-312 ameliorated AAD-related diarrhea symptoms by increasing the abundance of specific commensal microbiota. Interestingly, we demonstrated that these changes were coincident with the restoration of intestinal barrier function and enterocyte regeneration in AAD rats. In summary, we identified a potential probiotic therapeutic strategy for AAD and identified the vital roles of B. fragilis strain ZY-312 in modulating the colonic bacterial community and participating in microbiota-mediated epithelial cell proliferation and differentiation.

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Isolation and gut microbiota modulation of antibiotic-resistant probiotics from human feces

Cited by 7 publications

References 45 publications

H. pylori Eradication Treatment Alters Gut Microbiota and GLP-1 Secretion in Humans

H. pylori Eradication Treatment Alters Gut Microbiota and GLP-1 Secretion in Humans

Randomized, Controlled, Crossover trial of Prevention of Clindamycin‐Induced Gastrointestinal Signs Using a Synbiotic in Healthy Research Cats

Bacteroides fragilis Protects Against Antibiotic-Associated Diarrhea in Rats by Modulating Intestinal Defenses

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