Influence of Factors Altering Gastric Microbiota on Bariatric Surgery Metabolic Outcomes

The gut microbiota has been shown to have an impact on host metabolism. In the stomach, factors like proton pump inhibitor treatment and Helicobacter pylori haven been suggested to alter gut microbiota; however, the influence of these factors on the metabolic response to bariatric surgery has not been fully studied.

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Modification of the Gastric Mucosal Microbiota by a Strain-Specific Helicobacter pylori Oncoprotein and Carcinogenic Histologic Phenotype

mBio ◽

10.1128/mbio.00955-19 ◽

2019 ◽

Vol 10 (3) ◽

Cited By ~ 7

Author(s):

Jennifer M. Noto ◽

Joseph P. Zackular ◽

Matthew G. Varga ◽

Alberto Delgado ◽

Judith Romero-Gallo ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Community Structure ◽

Microbial Community ◽

Iron Deficiency ◽

Dependent Manner ◽

Content Type ◽

Β Diversity ◽

H Pylori ◽

Gastric Microbiota

ABSTRACT Helicobacter pylori is the strongest risk factor for gastric adenocarcinoma; however, most infected individuals never develop this malignancy. Strain-specific microbial factors, such as the oncoprotein CagA, as well as environmental conditions, such as iron deficiency, augment cancer risk. Importantly, dysbiosis of the gastric microbiota is also associated with gastric cancer. To investigate the combinatorial effects of these determinants in an in vivo model of gastric cancer, Mongolian gerbils were infected with the carcinogenic cag+ H. pylori strain 7.13 or a 7.13 cagA isogenic mutant, and microbial DNA extracted from gastric tissue was analyzed by 16S rRNA sequencing. Infection with H. pylori significantly increased gastric inflammation and injury, decreased α-diversity, and altered microbial community structure in a cagA-dependent manner. The effect of iron deficiency on gastric microbial communities was also investigated within the context of infection. H. pylori-induced injury was augmented under conditions of iron deficiency, but despite differences in gastric pathology, there were no significant differences in α- or β-diversity, phyla, or operational taxonomic unit (OTU) abundance among infected gerbils maintained on iron-replete or iron-depleted diets. However, when microbial composition was stratified based solely on the severity of histologic injury, significant differences in α- and β-diversity were present among gerbils harboring premalignant or malignant lesions compared to gerbils with gastritis alone. This study demonstrates that H. pylori decreases gastric microbial diversity and community structure in a cagA-dependent manner and that as carcinogenesis progresses, there are corresponding alterations in community structure that parallel the severity of disease. IMPORTANCE Microbial communities are essential for the maintenance of human health, and when these communities are altered, hosts can become susceptible to inflammation and disease. Dysbiosis contributes to gastrointestinal cancers, and specific bacterial species are associated with this phenotype. This study uses a robust and reproducible animal model to demonstrate that H. pylori infection induces gastric dysbiosis in a cagA-dependent manner and further that dysbiosis and altered microbial community structure parallel the severity of H. pylori-induced gastric injury. Ultimately, such models of H. pylori infection and cancer that can effectively evaluate multiple determinants simultaneously may yield effective strategies for manipulating the gastric microbiota to prevent the development of gastric cancer.

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Modulation of the gut microbiome: a systematic review of the effect of bariatric surgery

Acta Endocrinologica ◽

10.1530/eje-17-0403 ◽

2018 ◽

Vol 178 (1) ◽

pp. 43-56 ◽

Cited By ~ 63

Author(s):

Yan Guo ◽

Zhi-Ping Huang ◽

Chao-Qian Liu ◽

Lin Qi ◽

Yuan Sheng ◽

...

Keyword(s):

Systematic Review ◽

Bariatric Surgery ◽

Gut Microbiota ◽

Strong Evidence ◽

Gut Microbiome ◽

Animal Experiments ◽

Human Metabolism ◽

Microbial Groups ◽

Host Metabolism

Objective Bariatric surgery is recommended for patients with obesity and type 2 diabetes. Recent evidence suggested a strong connection between gut microbiota and bariatric surgery. Design Systematic review. Methods The PubMed and OVID EMBASE were used, and articles concerning bariatric surgery and gut microbiota were screened. The main outcome measures were alterations of gut microbiota after bariatric surgery and correlations between gut microbiota and host metabolism. We applied the system of evidence level to evaluate the alteration of microbiota. Modulation of short-chain fatty acid and gut genetic content was also investigated. Results Totally 12 animal experiments and 9 clinical studies were included. Based on strong evidence, 4 phyla (Bacteroidetes, Fusobacteria, Verrucomicrobia and Proteobacteria) increased after surgery; within the phylum Firmicutes, Lactobacillales and Enterococcus increased; and within the phylum Proteobacteria, Gammaproteobacteria, Enterobacteriales Enterobacteriaceae and several genera and species increased. Decreased microbial groups were Firmicutes, Clostridiales, Clostridiaceae, Blautia and Dorea. However, the change in microbial diversity is still under debate. Faecalibacterium prausnitzii, Lactobacillus and Coprococcus comes are implicated in many of the outcomes, including body composition and glucose homeostasis. Conclusions There is strong evidence to support a considerable alteration of the gut microbiome after bariatric surgery. Deeper investigations are required to confirm the mechanisms that link the gut microbiome and metabolic alterations in human metabolism.

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The Degree of Helicobacter pylori-Triggered Inflammation Is Manipulated by Preinfection Host Microbiota

Infection and Immunity ◽

10.1128/iai.00044-13 ◽

2013 ◽

Vol 81 (5) ◽

pp. 1382-1389 ◽

Cited By ~ 46

Author(s):

Annah S. Rolig ◽

Cynthia Cech ◽

Ethan Ahler ◽

J. Elliot Carter ◽

Karen M. Ottemann

Keyword(s):

Helicobacter Pylori ◽

Bacterial Communities ◽

Severe Disease ◽

Disease Outcome ◽

Gastric Tissue ◽

T Helper ◽

Content Type ◽

H Pylori ◽

Primary Risk Factor ◽

Gastric Microbiota

ABSTRACTHelicobacter pyloriinfects over 3 billion people worldwide and is the primary risk factor for gastric cancer. Most individuals infected withH. pyloridevelop only asymptomatic gastritis; however, some develop ulcers or gastric adenocarcinoma. We demonstrate that one previously unappreciated parameter influencingH. pyloridisease outcome is variation in the preinfection host microbiota. Utilizing a mouse model, we altered the microbiota by antibiotic treatment and found that these alterations resulted in significantly loweredH. pylori-triggered inflammation. Specifically, antibiotic pretreatment reduced CD4+T-helper cells andIfnγ transcript levels in gastric tissue afterH. pyloriinfection. The bacterial communities in mice with a reduced response toH. pyloridisplayed many differences from those in untreated mice, including significantly more cluster IV and XIVaClostridiumspp., bacteria known to influence inflammation via regulatory T cell populations. Our findings suggest that microbiota composition, perhapsClostridiumspp., contributes to the variable disease outcome ofH. pyloriinfection by altering the recruitment of CD4+T cells to the gastric compartment. Our results suggest that gastric microbiota could be used as a diagnostic tool to determine which patients are at risk for developing severe disease.

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Comparison of Amoxicillin?Metronidazole Plus Famotidine or Lansoprazole for Amoxicillin?Clarithromycin?Proton Pump Inhibitor Treatment Failures for Helicobacter pylori Infection

Helicobacter ◽

10.1111/j.1523-5378.2006.00435.x ◽

2006 ◽

Vol 11 (5) ◽

pp. 436-440 ◽

Cited By ~ 15

Author(s):

Kazunari Murakami ◽

Tadayoshi Okimoto ◽

Masaaki Kodama ◽

Ryugo Sato ◽

Hajime Miyajima ◽

...

Keyword(s):

Helicobacter Pylori ◽

Proton Pump Inhibitor ◽

Proton Pump ◽

Helicobacter Pylori Infection ◽

Proton Pump Inhibitor Treatment ◽

Inhibitor Treatment

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Inclusion of Konjac Flour in the Gestation Diet Changes the Gut Microbiota, Alleviates Oxidative Stress, and Improves Insulin Sensitivity in Sows

Applied and Environmental Microbiology ◽

10.1128/aem.01374-16 ◽

2016 ◽

Vol 82 (19) ◽

pp. 5899-5909 ◽

Cited By ~ 23

Author(s):

Chengquan Tan ◽

Hongkui Wei ◽

Jiangtao Ao ◽

Guang Long ◽

Jian Peng

Keyword(s):

Oxidative Stress ◽

Insulin Sensitivity ◽

Gut Microbiota ◽

Control Diet ◽

Rrna Gene ◽

Model Assessment ◽

Microbial Composition ◽

Content Type ◽

Konjac Flour ◽

Host Metabolism

ABSTRACTAlthough dietary fibers contribute to health and physiology primarily via the fermentative actions of the gut microbiota of the hosts, few studies have focused on how these interactions influence the metabolic status of sows. Here, the effects of inclusion of konjac flour (KF) in a gestation diet on oxidative stress status, insulin sensitivity, and gut microbiota were investigated to elucidate the correlation between the microbiota and metabolic changes in sows. Sows were assigned to either control or 2.2% KF dietary treatment during gestation. The gut microbiota population in sows during gestation and lactation was assessed by 16S rRNA gene sequencing. The oxidative stress parameters, homeostasis model assessment (HOMA) values, and fatty acids in the blood of sows were also assessed. Compared to the control diet group, KF significantly reduced the serum levels of reactive oxygen species (ROS) and 8-hydroxy-deoxyguanosine (8-OHdG) but increased the serum concentrations of glutathione peroxidase (GSH-Px) in sows on day 1 in lactation. Additionally, sows in the KF group had a lower HOMA insulin resistance value but a higher HOMA insulin sensitivity (HOMA-IS) value. KF induced changes in the gut microbial composition at the phylum and genus levels. The increased relative abundances ofAkkermansiaandRoseburiain the KF group were positively correlated with the HOMA-IS. Overall, dietary KF alleviated oxidative stress and improved insulin sensitivity of sows, and the changes in the gut microbiota in response to KF may have been correlated with the host metabolism response.IMPORTANCETo date, the effect of dietary fiber on metabolism responses and gut microbiota in sows has not been investigated. Here, KF supplementation of a gestation diet in sows was found to alleviate oxidative stress and to improve insulin sensitivity. Pyrosequencing analysis revealed that KF treatment induces changes in the gut microbiota composition at the phylum and genus levels. Moreover, the changes of gut microbiota in response to KF may be correlated with the host metabolism response.

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Eradicating Helicobacter pylori reduces hypergastrinaemia during long term omeprazole treatment

Gut ◽

10.1136/gut.42.2.159 ◽

1998 ◽

Vol 42 (2) ◽

pp. 159-165 ◽

Cited By ~ 18

Author(s):

A El-Nujumi ◽

C Williams ◽

J E Ardill ◽

K Oien ◽

K E L McColl

Keyword(s):

Helicobacter Pylori ◽

Proton Pump Inhibitor ◽

Proton Pump ◽

Serum Gastrin ◽

Symptomatic Treatment ◽

Initial Presentation ◽

Proton Pump Inhibitor Treatment ◽

H Pylori ◽

Inhibitor Treatment

Background—Both proton pump inhibitor drug treatment and Helicobacter pylori infection cause hypergastrinaemia in man.Aims—To determine whether eradicating H pylori is a means of reducing hypergastrinaemia during subsequent proton pump inhibitor treatment.Methods—Patients with H pylori were randomised to treatment with either anti-H pylori or symptomatic treatment. One month later, all received four weeks treatment with omeprazole 40 mg/day for one month followed by 20 mg/day for six months. Serum gastrin concentrations were measured before and following each treatment.Results—In the patients randomised to anti-H pylori treatment, eradication of the infection lowered median fasting gastrin by 48% and meal stimulated gastrin by 46%. When gastrin concentrations one month following anti-H pylori/symptomatic treatment were used as baseline, omeprazole treatment produced a similar percentage increase in serum gastrin in the H pylori infected and H pylorieradicated patients. Consequently, in the patients in which H pylori was not eradicated, median fasting gastrin concentration was 38 ng/l (range 26–86) at initial presentation and increased to 64 ng/l (range 29–271) after seven months omeprazole, representing a median increase of 68% (p<0.005). In contrast, in the patients randomised to H pylori eradication, median fasting gastrin at initial presentation was 54 ng/l (range 17–226) and was unchanged after seven months omeprazole at 38 ng/l (range 17–95).Conclusion—Eradicating H pylori is a means of reducing the rise in gastrin during subsequent long term omeprazole treatment. In view of the potential deleterious effects of hypergastrinaemia it may be appropriate to render patients H pylori negative prior to commencing long term proton pump inhibitor treatment.

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