Influence of bacteria on epigenetic gene control

Takahashi, Kyôko

doi:10.1007/s00018-013-1487-x

Cited by 62 publications

(54 citation statements)

References 70 publications

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“…Furthermore, as mentioned above, the TLR-4 function and expression are modulated not only by genetic variants and haplotypes [11,85,86] but also by environmental factors (such as diet [138][139][140][141], mite allergens [142], air pollution [143]), and their cross-interaction with microbiota [141], which may remain in a healthy state or show alterations (i.e. dysbiosis and consequent endotoxemia associated with age or obesity) [144,145]and consequent epigenetic changes [146,147]. Thus, many limitations and concerns emerge.…”

Section: Therapeutic Role Of Tlr-4 Pathway: From Experimental Data Tomentioning

confidence: 99%

Toll-like receptor-4 signaling pathway in aorta aging and diseases: “its double nature”

Balistreri

Ruvolo

Lio

et al. 2017

Journal of Molecular and Cellular Cardiology

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Section: Therapeutic Role Of Tlr-4 Pathway: From Experimental Data Tomentioning

confidence: 99%

Toll-like receptor-4 signaling pathway in aorta aging and diseases: “its double nature”

Balistreri

Ruvolo

Lio

et al. 2017

Journal of Molecular and Cellular Cardiology

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“…Epigenetic control of gene expression during a pathogenic bacterial infection is another important element in the regulation of host cell death. A recent report showed that many enteric bacterial pathogens, such as Salmonella typhimurium (17,18), Helicobacter pylori (19), and the enteropathogenic Escherichia coli (EPEC) (20), affect a diverse set of epigenetic factors such as DNA methylation and histone modification to regulate the selective activation or silencing of specific host genes (21). Thus, studies regarding the process leading to pathogen-induced cell death are likely to be critical to uncovering the mechanisms of pathogenesis.…”

mentioning

confidence: 99%

Vibrio vulnificus VvpE Stimulates IL-1β Production by the Hypomethylation of the IL-1β Promoter and NF-κB Activation via Lipid Raft–Dependent ANXA2 Recruitment and Reactive Oxygen Species Signaling in Intestinal Epithelial Cells

Lee

Jung

Song

et al. 2015

The Journal of Immunology

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An inflammatory response is a hallmark of necrosis evoked by bacterial pathogens. Vibrio vulnificus, VvpE, is an elastase that is responsible for tissue necrosis and inflammation; however, the molecular mechanism by which it regulates host cell death has not been characterized. In the present study, we investigate the cellular mechanism of VvpE with regard to host cell death and the inflammatory response of human intestinal epithelial (INT-407) cells. The recombinant protein (r)VvpE (50 pg/ml) caused cytotoxicity mainly via necrosis coupled with IL-1β production. The necrotic cell death induced by rVvpE is highly susceptible to the knockdown of annexin A (ANXA)2 and the sequestration of membrane cholesterol. We found that rVvpE induces the recruitment of NADPH oxidase 2 and neutrophil cytosolic factor 1 into membrane lipid rafts coupled with ANXA2 to facilitate the production of reactive oxygen species (ROS). The bacterial signaling of rVvpE through ROS production is uniquely mediated by the phosphorylation of redox-sensitive transcription factor NF-κB. The silencing of NF-κB inhibited IL-1β production during necrosis. rVvpE induced hypomethylation and region-specific transcriptional occupancy by NF-κB in the IL-1β promoter and has the ability to induce pyroptosis via NOD-, LRR-, and pyrin domain–containing 3 inflammasome. In a mouse model of V. vulnificus infection, the mutation of the vvpE gene from V. vulnificus negated the proinflammatory responses and maintained the physiological levels of the proliferation and migration of enterocytes. These results demonstrate that VvpE induces the hypomethylation of the IL-1β promoter and the transcriptional regulation of NF-κB through lipid raft–dependent ANXA2 recruitment and ROS signaling to promote IL-1β production in intestinal epithelial cells.

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“…Recent studies have shown that microbes affect a diverse set of epigenetic factors, including DNA methylation, histone modification, chromatin-associated complexes and non-coding RNAs, to alter chromatin structure and gene expression [76]. SCFAs have been reported to influence the epigenome; specifically, butyrate is recognised as a potent histone deacetylase inhibitor [66, 77].…”

Section: Mechanisms For Microbiome-induced Metabolic Disordersmentioning

confidence: 99%

Microbial transmission from mothers with obesity or diabetes to infants: an innovative opportunity to interrupt a vicious cycle

et al. 2016

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Maternal obesity and diabetes dramatically increase the long-term risk for obesity in the next generation, and pregnancy and lactation may be critical periods at which to aim primary prevention to break the obesity cycle. It is becoming increasingly clear that the gut microbiome in newborns and infants plays a significant role in gut health and therefore child development. Alteration of the early infant gut microbiome has been correlated with the development of childhood obesity and autoimmune conditions, including asthma, allergies and, more recently, type 1 diabetes. This is likely to be due to complex interactions between mode of delivery, antibiotic use, maternal diet, components of breastfeeding and a network of regulatory events involving both the innate and adaptive immune systems within the infant host. Each of these factors are critical for informing microbiome development and can affect immune signalling, toxin release and metabolic signals, including short-chain fatty acids and bile acids, that regulate appetite, metabolism and inflammation. In several randomised controlled trials, probiotics have been administered with the aim of targeting the microbiome during pregnancy to improve maternal and infant health but the findings have often been confounded by mode of delivery, antibiotic use, ethnicity, infant sex, maternal health and length of exposure. Understanding how nutritional exposure, including breast milk, affects the assembly and development of both maternal and infant microbial communities may help to identify targeted interventions during pregnancy and in infants born to mothers with obesity or diabetes to slow the transmission of obesity risk to the next generation. The aim of this review is to discuss influences on infant microbiota colonisation and the mechanism(s) underlying how alterations due to maternal obesity and diabetes may lead to increased risk of childhood obesity.

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Influence of bacteria on epigenetic gene control

Cited by 62 publications

References 70 publications

Toll-like receptor-4 signaling pathway in aorta aging and diseases: “its double nature”

Toll-like receptor-4 signaling pathway in aorta aging and diseases: “its double nature”

Vibrio vulnificus VvpE Stimulates IL-1β Production by the Hypomethylation of the IL-1β Promoter and NF-κB Activation via Lipid Raft–Dependent ANXA2 Recruitment and Reactive Oxygen Species Signaling in Intestinal Epithelial Cells

Microbial transmission from mothers with obesity or diabetes to infants: an innovative opportunity to interrupt a vicious cycle

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