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Author (up) Chen, X.; D'Souza, R.; Hong, S.-T. file  url
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  Title The role of gut microbiota in the gut-brain axis: current challenges and perspectives Type Journal Article
  Year 2013 Publication Protein & Cell Abbreviated Journal Protein Cell  
  Volume 4 Issue 6 Pages 403-414  
  Keywords Brain/*metabolism; Central Nervous System/metabolism; Gastrointestinal Tract/*metabolism/microbiology; High-Throughput Nucleotide Sequencing; Humans; Liver/metabolism; Metabolic Diseases/metabolism/pathology; *Metagenome; Microbiome; Receptors, G-Protein-Coupled/metabolism  
  Abstract Brain and the gastrointestinal (GI) tract are intimately connected to form a bidirectional neurohumoral communication system. The communication between gut and brain, knows as the gut-brain axis, is so well established that the functional status of gut is always related to the condition of brain. The researches on the gut-brain axis were traditionally focused on the psychological status affecting the function of the GI tract. However, recent evidences showed that gut microbiota communicates with the brain via the gut-brain axis to modulate brain development and behavioral phenotypes. These recent findings on the new role of gut microbiota in the gut-brain axis implicate that gut microbiota could associate with brain functions as well as neurological diseases via the gut-brain axis. To elucidate the role of gut microbiota in the gut-brain axis, precise identification of the composition of microbes constituting gut microbiota is an essential step. However, identification of microbes constituting gut microbiota has been the main technological challenge currently due to massive amount of intestinal microbes and the difficulties in culture of gut microbes. Current methods for identification of microbes constituting gut microbiota are dependent on omics analysis methods by using advanced high tech equipment. Here, we review the association of gut microbiota with the gut-brain axis, including the pros and cons of the current high throughput methods for identification of microbes constituting gut microbiota to elucidate the role of gut microbiota in the gut-brain axis.  
  Call Number Serial 2005  
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Author (up) Pikarsky, E.; Porat, R.M.; Stein, I.; Abramovitch, R.; Amit, S.; Kasem, S.; Gutkovich-Pyest, E.; Urieli-Shoval, S.; Galun, E.; Ben-Neriah, Y. file  url
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  Title NF-kappaB functions as a tumour promoter in inflammation-associated cancer Type Journal Article
  Year 2004 Publication Nature Abbreviated Journal Nature  
  Volume 431 Issue 7007 Pages 461-466  
  Keywords ATP Binding Cassette Transporter, Sub-Family B/deficiency/genetics; ATP-Binding Cassette Transporters/genetics; Animals; Carcinoma, Hepatocellular/*complications/etiology/*metabolism/pathology; Chronic Disease; Disease Progression; Hepatitis/complications/etiology/metabolism/pathology; Hepatocytes/metabolism/pathology; I-kappa B Proteins/metabolism; Inflammation/*complications/*metabolism/pathology; Liver/metabolism/pathology; Mice; Mice, Knockout; NF-kappa B/*metabolism; Paracrine Communication; Tumor Necrosis Factor-alpha/metabolism  
  Abstract The causes of sporadic human cancer are seldom recognized, but it is estimated that carcinogen exposure and chronic inflammation are two important underlying conditions for tumour development, the latter accounting for approximately 20% of human cancer. Whereas the causal relationship between carcinogen exposure and cancer has been intensely investigated, the molecular and cellular mechanisms linking chronic inflammation to tumorigenesis remain largely unresolved. We proposed that activation of the nuclear factor kappaB (NF-kappaB), a hallmark of inflammatory responses that is frequently detected in tumours, may constitute a missing link between inflammation and cancer. To test this hypothesis, we studied the Mdr2-knockout mouse strain, which spontaneously develops cholestatic hepatitis followed by hepatocellular carcinoma, a prototype of inflammation-associated cancer. We monitored hepatitis and cancer progression in Mdr2-knockout mice, and here we show that the inflammatory process triggers hepatocyte NF-kappaB through upregulation of tumour-necrosis factor-alpha (TNFalpha) in adjacent endothelial and inflammatory cells. Switching off NF-kappaB in mice from birth to seven months of age, using a hepatocyte-specific inducible IkappaB-super-repressor transgene, had no effect on the course of hepatitis, nor did it affect early phases of hepatocyte transformation. By contrast, suppressing NF-kappaB inhibition through anti-TNFalpha treatment or induction of IkappaB-super-repressor in later stages of tumour development resulted in apoptosis of transformed hepatocytes and failure to progress to hepatocellular carcinoma. Our studies thus indicate that NF-kappaB is essential for promoting inflammation-associated cancer, and is therefore a potential target for cancer prevention in chronic inflammatory diseases.  
  Call Number Serial 2053  
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