Deep sequencing reveals microbiota dysbiosis of tongue coat in patients with liver carcinoma

Lü, Haifeng; Ren, Zhigang; Li, Ang; Zhang, Hua; Jiang, Jianwen; Xu, Shaoyan; Luo, Qixia; Zhou, Kai; Sun, Xiaoli; Zheng, Shusen

doi:10.1038/srep33142

Cited by 96 publications

(108 citation statements)

References 42 publications

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“…It is therefore postulated oral bacterial overgrowth may have a profound effect on intestinal bacterial communities and thus CLD pathogenesis and HCC development. This concept is supported by a recent study that showed a high level of oral microbiota Oribacterium and Fusobacterium in HCC patients [13]. The alteration in gut microbiota composition in HCC is summarized in Table 1.…”

Section: Gut Dysbiosissupporting

confidence: 56%

“…Microbial gene signatures that relate to energy production, nickel/iron transport, and amino acid transport appear to be altered in HCC patients when compared to healthy controls [13]. Moreover, when compared to cirrhotic patients, fecal samples from HCC patients have shown increased growth of phylum Actinobacteria and 13 genera including Gemmiger and Parabacteroides [14].…”

Section: Gut Dysbiosismentioning

confidence: 98%

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Microbiota, Inflammation, and Gut Barrier Dysfunction in HCC

Ram¹,

Wright²,

Vairappan³

2021

Liver Pathology

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Hepatocellular carcinoma (HCC), which represents 90% of all primary liver cancers, is the fifth most common cancer and the third cause of cancer mortality rate. It is a complex disease with a poor prognosis. Incidence and mortality rates are increasing in many geographical regions, indicating a need for better management strategies. Chronic inflammation is the major driving factors for HCC development, which typically develops on the background of chronic liver disease (CLD). Currently, a large body of literature has focused on the key role of the gut-liver axis as the major pathophysiological mechanism of hepatic disease severity and HCC development. This chapter will describe the role of gut microbiota, inflammation, and intestinal barrier dysfunction-associated mechanism in the progression of HCC. In particular, enteric dysbiosis, tight junction, and inflammatory mediators in the pathogenesis of liver cancer will be discussed. Furthermore, this chapter will identify the possible potential therapeutic approach for the control of gut bacterial overgrowth, inflammation and restoration of eubiosis, and tight junction integrity in HCC.

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Section: Gut Dysbiosissupporting

confidence: 56%

Section: Gut Dysbiosismentioning

confidence: 98%

Microbiota, Inflammation, and Gut Barrier Dysfunction in HCC

Ram¹,

Wright²,

Vairappan³

2021

Liver Pathology

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“…[43] High-throughput sequencing was performed on an Illumina MiSeq instrument according to the manufacturer's instructions. [43] High-throughput sequencing was performed on an Illumina MiSeq instrument according to the manufacturer's instructions.…”

Section: Methodsmentioning

confidence: 99%

Gut Microbiota Changes in Patients with Bipolar Depression

et al. 2019

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This study aims to characterize the gut microbiota in depressed patients with bipolar disorder (BD) compared with healthy controls (HCs), to examine the effects of quetiapine treatment on the microbiota, and to explore the potential of microbiota as a biomarker for BD diagnosis and treatment outcome. Analysis of 16S‐ribosomal RNA gene sequences reveals that gut microbial composition and diversity are significantly different between BD patients and HCs. Phylum Bacteroidetes and Firmicutes are the predominant bacterial communities in BD patients and HCs, respectively. Lower levels of butyrate‐producing bacteria are observed in untreated patients. Microbial composition changes following quetiapine treatment in BD patients. Notably, 30 microbial markers are identified on a random forest model and achieve an area under the curve (AUC) of 0.81 between untreated patients and HCs. Ten microbial markers are identified with the AUC of 0.93 between responder and nonresponder patients. This study characterizes the gut microbiota in BD and is the first to evaluate microbial changes following quetiapine monotherapy. Gut microbiota‐based biomarkers may be helpful in BD diagnosis and predicting treatment outcome, which need further validations.

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“…forsythia expresses two sialidases, SiaHI and NanH, which are important in bacterial colonization [11]. Oral microbiome composition alters fatty acid metabolism [12] and are not just associated with oral cancer development [13] but also are suspected of promoting esophageal [14,15], pancreatic cancer [16,17], or liver cancer [18]. T. forsythia "contributes to the growth of a partner species, Fusobacterium nucleatum, in co-biofilms" [19].…”

Section: Microbiome (Tab 1)mentioning

confidence: 99%

Microbiome and morbid obesity increase pathogenic stimulus diversity

Brücher

Jamall

2019

4open

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The microbiome, the relationship between environmental factors, a high-fat diet, morbid obesity, and host response have been associated with cancer, only a small fraction of which (<10%) are genetically triggered. This nongenetic association is underpinned by a worldwide increase in morbid obesity, which is associated with both insulin resistance and chronic inflammation. The connection of the microbiome and morbid obesity is reinforced by an approximate shift of about 47% in the estimated total number of bacteria and an increase from 38,000,000,000,000 in a reference man to 56,000,000,000,000 in morbid obesity leading to a disruption of the microbial ecology within the gut. Humans contain 6,000,000,000 microbes and more than 90% of the cells of the human body are microorganisms. Changes in the microflora of the gut are associated with the polarization of ion channels by butyrate, thereby influencing cell growth. The decrease in the relative proportion of Bacteroidetes together with a change in the fermentation of carbohydrates by bacteria is observed in morbid obesity. The disruption of homeostasis of the microflora in the obese changes signaling and crosstalk of several pathways, resulting in inflammation while suppressing apoptosis. The interactions between the microbiome and morbid obesity are important to understand signaling and crosstalk in the context of the progression of the six-step sequence of carcinogenesis. This disruption of homeostasis increases remodeling of the extracellular matrix and fibrosis followed by the none-resolvable precancerous niche as the internal pathogenic stimuli continue. The chronic stress explains why under such circumstances there is a greater proclivity for normal cells to undergo the transition to cancer cells.

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Deep sequencing reveals microbiota dysbiosis of tongue coat in patients with liver carcinoma

Cited by 96 publications

References 42 publications

Microbiota, Inflammation, and Gut Barrier Dysfunction in HCC

Microbiota, Inflammation, and Gut Barrier Dysfunction in HCC

Gut Microbiota Changes in Patients with Bipolar Depression

Microbiome and morbid obesity increase pathogenic stimulus diversity

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