Effect of trimethylamine N-oxide on inflammation and the gut microbiota in Helicobacter pylori-infected mice

Wu, Daoyan; Cao, Mei; Li, Ningzhe; Zhang, Andong; Yu, Zuwei; Cheng, Juan; Xie, Xuemei; Wang, Zeyu; Lu, Shaofei; Shi, Yan; Zhou, Jie; Peng, Jingshan; Zhao, Jian

doi:10.1016/j.intimp.2019.106026

Cited by 16 publications

(13 citation statements)

References 48 publications

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“…The abundance of Blautia, Eubacterium rectale, and Bifidobacterium was also negatively correlated with systolic BP [26,27]. The PE-enriched genera Escherichia Shigella and Enterobacter, both of which comprise Gram-negative bacteria that can produce a large amount of LPS, were previously reported to cause excessive inflammatory responses [28,29]. Combined with these previous reports, our current findings of disturbances in the relative abundance of the GM in patients with PE suggested that GM dysbiosis may be important for PE pathogenesis.…”

Section: Discussionsupporting

confidence: 77%

Short-chain fatty acids accompanying changes in the gut microbiome contribute to the development of hypertension in patients with preeclampsia

et al. 2020

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Preeclampsia (PE) is regarded as a pregnancy-associated hypertension disorder that is related to excessive inflammatory responses. Although the gut microbiota (GM) and short-chain fatty acids (SCFAs) have been related to hypertension, their effects on PE remain unknown. We determined the GM abundance and faecal SCFA levels by 16S ribosomal RNA (rRNA) sequencing and gas chromatography, respectively, using faecal samples from 27 patients with severe PE and 36 healthy, pregnant control subjects. We found that patients with PE had significantly decreased GM diversity and altered GM abundance. At the phylum level, patients with PE exhibited decreased abundance of Firmicutes albeit increased abundance of Proteobacteria; at the genus level, patients with PE had lower abundance of Blautia, Eubacterium_rectale, Eubacterium_hallii, Streptococcus, Bifidobacterium, Collinsella, Alistipes, and Subdoligranulum, albeit higher abundance of Enterobacter and Escherichia_Shigella. The faecal levels of butyric and valeric acids were significantly decreased in patients with PE and significantly correlated with the above-mentioned differential GM abundance. We predicted significantly increased abundance of the lipopolysaccharide (LPS)-synthesis pathway and significantly decreased abundance of the G protein-coupled receptor (GPCR) pathway in patients with PE, based on phylogenetic reconstruction of unobserved states (PICRUSt). Finally, we evaluated the effects of oral butyrate on LPS-induced hypertension in pregnant rats. We found that butyrate significantly reduced the blood pressure (BP) in these rats. In summary, we provide the first evidence linking GM dysbiosis and reduced faecal SCFA to PE and demonstrate that butyrate can directly regulate BP in vivo, suggesting its potential as a therapeutic agent for PE.

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Section: Discussionsupporting

confidence: 77%

Short-chain fatty acids accompanying changes in the gut microbiome contribute to the development of hypertension in patients with preeclampsia

et al. 2020

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“…Thus, trimethylamine N-oxide enhanced H. pylori virulence by upregulating the expression of the virulence gene encoding CagA. The authors also confirmed that the intake of trimethylamine enhanced the production of inflammatory markers and reduced the richness and diversity of the intestinal microbiota [ 77 ]. Similar results suggested that the treatment of infected mice with choline aggravated both the inflammation produced by the bacteria itself and the alteration of the intestinal microbiota [ 78 ].…”

Section: The Impact Of Diet Patterns In Helicobacter Pylori Infectionmentioning

confidence: 87%

Impact of Dietary Patterns on H. pylori Infection and the Modulation of Microbiota to Counteract Its Effect. A Narrative Review

et al. 2021

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Helicobacter pylori (H. pylori) is a Gram-negative bacterium that colonizes the stomach and can induce gastric disease and intra-gastric lesions, including chronic gastritis, peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. This bacterium is responsible for long-term complications of gastric disease. The conjunction of host genetics, immune response, bacterial virulence expression, diet, micronutrient availability, and microbiome structure influence the disease outcomes related to chronic H. pylori infection. In this regard, the consumption of unhealthy and unbalanced diets can induce microbial dysbiosis, which infection with H. pylori may contribute to. However, to date, clinical trials have reported controversial results and current knowledge in this field is inconclusive. Here, we review preclinical studies concerning the changes produced in the microbiota that may be related to H. pylori infection, as well as the involvement of diet. We summarize and discuss the last approaches based on the modulation of the microbiota to improve the negative impact of H. pylori infection and their potential translation from bench to bedside.

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“…The corresponding gene expression and relative mRNA expression were evaluated by the 2‐ΔΔcq method and geometric mean results. The primers for RT‐qPCR were obtained from Primer Bank and designed via Primer‐BLAST, and they are listed in Table 19 …”

Section: Methodsmentioning

confidence: 99%

Effects of sodium butyrate supplementation on inflammation, gut microbiota, and short‐chain fatty acids in Helicobacter pylori‐infected mice

Huang

Ding

et al. 2021

Helicobacter

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Background Inflammation induced by Helicobacter pylori (H. pylori) infection is the basis for the pathogenesis of H. pylori. Butyric acid, a diet‐related microbial‐associated metabolite, is connected to inflammation, metabolic syndrome, and other diseases. Several studies have indicated the effects of sodium butyrate (SB) against bacteria; however, the effects of SB on the main virulence factors of H. pylori, H. pylori‐induced inflammation, and gut microbiota composition remain unclear. Materials and Methods SB was supplemented in H. pylori coculture and administered to mice infected with H. pylori. The effects of SB intake on inflammation, gut microbiota composition, and short‐chain fatty acids (SCFAs) in H. pylori‐infected mice were assessed. Results The in vitro experiments demonstrated that SB not only inhibited the growth of H. pylori but also decreased the mRNA expression of CagA and VacA. SB intake reduced the production of virulence factors in H. pylori‐infected mice, inhibited the IκBα/NF‐κB pathway by reducing the expression of Toll‐like receptors (TLRs), and reduced the production of TNF‐α and IL‐8. Further analysis demonstrated that H. pylori infection altered the relative abundance of the intestinal microbial community in mice. The level of SCFAs in the feces of H. pylori‐infected mice was changed, although the intake of SB did not obviously change the level of SCFAs. Conclusions Our study showed that SB may decrease H. pylori‐induced inflammation by inhibiting the viability and virulence of H. pylori and may reduce inflammation in association with the gut microbiota in H. pylori‐infected mice. This study may provide novel insights into the mechanisms by which SB, a diet‐related microbial‐associated metabolite, affects H. pylori‐induced disease development.

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Effect of trimethylamine N-oxide on inflammation and the gut microbiota in Helicobacter pylori-infected mice

Cited by 16 publications

References 48 publications

Short-chain fatty acids accompanying changes in the gut microbiome contribute to the development of hypertension in patients with preeclampsia

Short-chain fatty acids accompanying changes in the gut microbiome contribute to the development of hypertension in patients with preeclampsia

Impact of Dietary Patterns on H. pylori Infection and the Modulation of Microbiota to Counteract Its Effect. A Narrative Review

Effects of sodium butyrate supplementation on inflammation, gut microbiota, and short‐chain fatty acids in Helicobacter pylori‐infected mice

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