scholarly journals Dietary sulfate-driven and gut dysbiosis-triggered breast cancer-related gene upregulation

2018 ◽  
Author(s):  
CHEN YanPingf ◽  
LIAO Tao ◽  
TAN LiLi ◽  
CHEN DongMei ◽  
XU Qin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gut Microbiota ◽  
Individual Difference ◽  
Suppressor Gene ◽  
Low Grade ◽  
Ki 67 ◽  
Cancer Related Gene ◽  
The Individual ◽  
Low Grade Inflammation ◽  
Gut Microbiota Dysbiosis

AbstractBy gut microbiota metagenomic analysis, we found that the abundance of sulfatase-secreting bacteria (SSB) in the gut of mice fed chondroitin sulfate (CS) increases with significant individual difference. The fluctuation of lipopolysaccharide (LPS) and pro-inflammatory indicators with significant individual and tissue variations was also observed. After mice were fed mixed with CS or injected separately with LPS, the breast cancer-related transcriptional factor genes, BCL11A and RUNX1, were upregulated, whereas the tumor suppressor gene, TP53BP1, were downregulated. Further, the mammary myopithelium marker CK5/6, the mammary hyperplasia marker Ki-67, and other tumor markers were also upregulated. While the exogenous estradiol does not induce the expression of BCL11A, RUNX1, and TP53BP1, the estrogen receptor (ER) agonist Fulvestrant that mimics estradiol action not only elevates estradiol concentrations, but also upregulates tumor marker expression levels, revealing that ER inflammatory inactivation and hyperestrogenemia induction might be the etiological cues of breast cancer origin. This study has preliminarily established a possible correlation of gut microbiota dysbiosis and chronic low-grade inflammation with the early-phase onset of breast cancer in mice. The statistical insignificance of test data was attributed to the individual difference of gut microbiota compositions, which determining the individual and tissue variations of systemic inflammation.

Evidence from comparative genomic analyses indicating that Lactobacillus-mediated irritable bowel syndrome alleviation is mediated by the conjugated linoleic acid synthesis

2021 ◽  
Author(s):  
Yang Liu ◽  
Wei Xiao ◽  
Leilei Yu ◽  
Fengwei Tian ◽  
Gang Wang ◽  
...  
Keyword(s):  
Irritable Bowel Syndrome ◽  
Linoleic Acid ◽  
Gut Microbiota ◽  
Acid Synthesis ◽  
Comparative Genomic ◽  
Low Grade ◽  
Genomic Analyses ◽  
Irritable Bowel ◽  
Low Grade Inflammation ◽  
Gut Microbiota Dysbiosis

Irritable bowel syndrome (IBS) is a chronic intestinal disorder accompanied by low-grade inflammation, visceral hypersensitivity, and gut microbiota dysbiosis. Several studies have indicated that Lactobacillus supplementation can help to alleviate...

Regulation of Metabolism: A Cross Talk Between Gut Microbiota and Its Human Host

Physiology ◽  
2012 ◽  
Vol 27 (5) ◽  
pp. 300-307 ◽  
Author(s):  
Rémy Burcelin
Keyword(s):  
Immune System ◽  
Gut Microbiota ◽  
Low Grade ◽  
Gene Products ◽  
Individual Level ◽  
Obesity And Diabetes ◽  
Regulation Of Metabolism ◽  
Molecular Origin ◽  
The Individual ◽  
Low Grade Inflammation

The recent epidemic of obesity and diabetes and the diversity at the individual level could be explained by the intestinal microbiota-to-host relationship. More than four million gene products from the microbiome could interact with the immune system to induce a tissue metabolic infection, which is the molecular origin of the low-grade inflammation that characterizes the onset of obesity and diabetes.

scholarly journals Inflammation-Related Mechanisms in Chronic Kidney Disease Prediction, Progression, and Outcome

2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Simona Mihai ◽  
Elena Codrici ◽  
Ionela Daniela Popescu ◽  
Ana-Maria Enciu ◽  
Lucian Albulescu ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Gut Microbiota ◽  
Clinical Care ◽  
Low Grade ◽  
Public Health Burden ◽  
Inflammatory Status ◽  
Low Grade Inflammation ◽  
Gut Microbiota Dysbiosis

Persistent, low-grade inflammation is now considered a hallmark feature of chronic kidney disease (CKD), being involved in the development of all-cause mortality of these patients. Although substantial improvements have been made in clinical care, CKD remains a major public health burden, affecting 10–15% of the population, and its prevalence is constantly growing. Due to its insidious nature, CKD is rarely diagnosed in early stages, and once developed, its progression is unfortunately irreversible. There are many factors that contribute to the setting of the inflammatory status in CKD, including increased production of proinflammatory cytokines, oxidative stress and acidosis, chronic and recurrent infections, altered metabolism of adipose tissue, and last but not least, gut microbiota dysbiosis, an underestimated source of microinflammation. In this scenario, a huge step forward was made by the increasing progression of omics approaches, specially designed for identification of biomarkers useful for early diagnostic and follow-up. Recent omics advances could provide novel insights in deciphering the disease pathophysiology; thus, identification of circulating biomarker panels using state-of-the-art proteomic technologies could improve CKD early diagnosis, monitoring, and prognostics. This review aims to summarize the recent knowledge regarding the relationship between inflammation and CKD, highlighting the current proteomic approaches, as well as the inflammasomes and gut microbiota dysbiosis involvement in the setting of CKD, culminating with the troubling bidirectional connection between CKD and renal malignancy, raised on the background of an inflammatory condition.

Modulation of gut microbiota by Mantequilla and Melipona honeys decrease low-grade inflammation caused by high fructose corn syrup or sucrose in rats

2021 ◽  
pp. 110856
Author(s):  
Diana Coutiño-Hernández ◽  
Mónica Sánchez-Tapia ◽  
Francisco Leal-Vega ◽  
Miriam Bobadilla del Valle ◽  
Héctor Ledezma ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Low Grade ◽  
High Fructose Corn Syrup ◽  
Corn Syrup ◽  
High Fructose ◽  
Low Grade Inflammation

scholarly journals Amelioration of metabolic syndrome by metformin associates with reduced indices of low-grade inflammation independently of the gut microbiota

2019 ◽  
Vol 317 (6) ◽  
pp. E1121-E1130 ◽  
Author(s):  
Aneseh Adeshirlarijaney ◽  
Jun Zou ◽  
Hao Q. Tran ◽  
Benoit Chassaing ◽  
Andrew T. Gewirtz
Keyword(s):  
Metabolic Syndrome ◽  
Gut Microbiota ◽  
Early Stage ◽  
Mechanisms Of Action ◽  
Low Grade ◽  
Inflammatory Agent ◽  
Frontline Treatment ◽  
Anti Inflammatory ◽  
Low Grade Inflammation

Metformin beneficially impacts several aspects of metabolic syndrome including dysglycemia, obesity, and liver dysfunction, thus making it a widely used frontline treatment for early-stage type 2 diabetes, which is associated with these disorders. Several mechanisms of action for metformin have been proposed, including that it acts as an anti-inflammatory agent, possibly as a result of its impact on intestinal microbiota. In accord with this possibility, we observed herein that, in mice with diet-induced metabolic syndrome, metformin impacts the gut microbiota by preventing its encroachment upon the host, a feature of metabolic syndrome in mice and humans. However, the ability of metformin to beneficially impact metabolic syndrome in mice was not markedly altered by reduction or elimination of gut microbiota, achieved by the use of antibiotics or germfree mice. Although reducing or eliminating microbiota by itself suppressed diet-induced dysglycemia, other features of metabolic syndrome including obesity, hepatic steatosis, and low-grade inflammation remained suppressed by metformin in the presence or absence of gut microbiota. These results support a role for anti-inflammatory activity of metformin, irrespective of gut microbiota, in driving some of the beneficial impacts of this drug on metabolic syndrome.

scholarly journals ECRG4 acts as a tumor suppressor gene frequently hypermethylated in human breast cancer

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Gao-Yan Tang ◽  
Guo-Jun Tang ◽  
Lu Yin ◽  
Chen Chao ◽  
Ren Zhou ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Suppressor ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Human Breast Cancer ◽  
Suppressor Gene ◽  
Human Breast ◽  
Cancer Related Gene ◽  
And Migration ◽  
Gene 4

Abstract Human breast cancer is a malignant form of tumor with a relatively high mortality rate. Although esophageal cancer-related gene 4 (ECRG4) is thought to be a possible potent tumor suppressor gene that acts to suppress breast cancer, its precise role in this disease is not understood. Herein, we assess the correlation between ECRG4 expression and DNA methylation, probing the potential epigenetic regulation of ECRG4 in breast cancer. We analyzed ECRG4 promoter methylation via methylation-specific PCR (MSPCR), bisulfite sequencing, and a promoter reporter assay in human breast cancer cell lines and samples. Gene expression was assessed by quantitative real-time PCR (qPCR), while protein levels were assessed by Western blotting. CCK8 assays were used to quantify cell growth; Esophageal cancer-related gene 4 wound healing assays were used to assess cellular migration, while flow cytometry was used to assess apoptosis and cell cycle progression. Apoptosome formation was validated via CO-IP and Western blotting. We found that human breast cancer samples exhibited increased methylation of the ECRG4 promoter and decreased ECRG4 expression. Remarkably, the down-regulation of ECRG4 was highly associated with promoter methylation, and its expression could be re-activated via 5-aza-2′-deoxycytidine treatment to induce demethylation. ECRG4 overexpression impaired breast cancer cell proliferation and migration, and led to G0/G1 cell cycle phase arrest. Moreover, ECRG4 induced the formation of the Cytc/Apaf-1/caspase-9 apoptosome and promoted breast cancer cell apoptosis. ECRG4 is silenced in human breast cancer cells and cell lines, likely owing to promoter hypermethylation. ECRG4 may act as a tumor suppressor, inhibiting proliferation and migration, inducing G0/G1 phase arrest and apoptosis via the mitochondrial apoptotic pathway.

scholarly journals Cartilage-gut-microbiome axis: a new paradigm for novel therapeutic opportunities in osteoarthritis

RMD Open ◽  
2019 ◽  
Vol 5 (2) ◽  
pp. e001037 ◽  
Author(s):  
Jean-Marie Berthelot ◽  
Jérémie Sellam ◽  
Yves Maugars ◽  
Francis Berenbaum
Keyword(s):  
Gut Microbiota ◽  
Gut Microbiome ◽  
Cartilage Degradation ◽  
Low Grade ◽  
New Paradigm ◽  
Healthy Human ◽  
Human Cartilage ◽  
Intact Cartilage ◽  
Low Grade Inflammation

DNA of gut microbiota can be found in synovium of osteoarthritis and rheumatoid arthritis. This finding could result from the translocation of still alive bacteria from gut to joints through blood, since the diversified dormant microbiota of healthy human blood can be transiently resuscitated in vitro. The recent finding of gut microbiome in human cartilage, which differed between osteoarthritis and controls, suggests that a similar trafficking of dead or alive bacteria from gut microbiota physiologically occurs between gut and epiphysial bone marrow. Subchondral microbiota could enhance cartilage healing and transform components of deep cartilage matrix in metabolites with immunosuppressive properties. The differences of microbiome observed between hip and knee cartilage, either in osteoarthritis or controls, might be the counterpart of subtle differences in chondrocyte metabolism, themselves in line with differences in DNA methylation according to joints. Although bacteria theoretically cannot reach chondrocytes from the surface of intact cartilage, some bacteria enter the vascular channels of the epiphysial growth cartilage in young animals, whereas others can infect chondrocytes in vitro. In osteoarthritis, the early osteochondral plate angiogenesis may further enhance the ability of microbiota to locate close to the deeper layers of cartilage, and this might lead to focal dysbiosis, low-grade inflammation, cartilage degradation, epigenetic changes in chondrocytes and worsening of osteoarthritis. More studies on cartilage across different ethnic groups, weights, and according to age, are needed, to confirm the silent presence of gut microbiota close to human cartilage and better understand its physiologic and pathogenic significance.

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