Figure 3 The 'leaky gut' hypothesis

Slides:



Advertisements
Similar presentations
What’s All the Fuss About the Microbiome?
Advertisements

Volume 141, Issue 5, Pages (November 2011)
Volume 141, Issue 5, Pages (November 2011)
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 3 Low-grade inflammation in FGID
Figure 4 The gut microbiota directly influences T-cell differentiation
Figure 3 Neutrophils in liver inflammation
Figure 4 Interactions between adipose, the microbiome and kidney
Figure 1 Differential immune responses in the gut (oral tolerance)
Figure 1 Contribution of the gut microbiota
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 3 The fat–intestine–kidney axis
Figure 1 Gut microorganisms at the intersection of several diseases
Figure 5 Lipid droplet consumption
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 2 The microbiome–gut–brain axis
Volume 141, Issue 5, Pages (November 2011)
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Endocrinol. doi: /nrendo
The gut microbiota and the liver
Figure 4 Tumour-induced neutrophil extracellular trap
Figure 1 Schematic outlining the results of Buffington et al.
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 3 Polysaccharides from plants and mushrooms
Figure 4 Proinflammatory immune cells and their crosstalk in patients with IBD Figure 4 | Proinflammatory immune cells and their crosstalk in patients.
Figure 1 Definition and concept of ACLF
Figure 1 Functions, features and phenotypes of HSCs in normal and diseased livers Figure 1 | Functions, features and phenotypes of HSCs in normal and diseased.
Figure 4 The gut–kidney axis, inflammation and cardiovascular disease in CKD Figure 4 | The gut–kidney axis, inflammation and cardiovascular disease in.
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
David L. McCollum, J. Martin Rodriguez 
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 5 Intestinal lymph draining pattern and contents
Figure 1 An overview of the TIMER microbiota–host
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
to the liver and promote patient-derived xenograft tumour growth
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 2 13C-octanoic acid gastric emptying breath test
Figure 5 Chrononutrition in the liver
Figure 2 Key brain–immune–gut interactions
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 2 Three distinct paracellular epithelial
Figure 1 Key mechanistic pathways involved in the gut–liver axis in NAFLD progression Figure 1 | Key mechanistic pathways involved in the gut–liver axis.
Figure 6 Possible therapeutic targets to decrease hepatic steatosis
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 1 Influence of diet on gut microbiota and blood pressure
Figure 1 Animal models of liver regeneration
Figure 4 The gut–liver relationship in PSC
Figure 2 Pro-inflammatory and anti-inflammatory effects of the gut microbiota Figure 2 | Pro-inflammatory and anti-inflammatory effects of the gut microbiota.
Figure 3 Strategies to improve liver regeneration
The National Biome Initiative: An allergy perspective
Figure 1 Brain–gut axis Brain–gut axis. Schematic of the brain–gut axis, including inputs from the gut microbiota, the ENS, the immune system and the external.
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 2 New therapeutic approaches in IBD with their specific targets
Figure 5 Systems biological model of IBS
Figure 2 The hypoxia-induced proinflammatory
Figure 4 Local species pools that contribute to the
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Hans-Joachim Anders, Kirstin Andersen, Bärbel Stecher 
Figure 1 New therapeutic approaches in IBD therapy based on blockade of T-cell homing and retention Figure 1 | New therapeutic approaches in IBD therapy.
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Figure 2 Lifelong influences on the gut microbiome from
The Gastrointestinal Tumor Microenvironment
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Inflammatory pathways in alcoholic steatohepatitis
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Presentation transcript:

Figure 3 The 'leaky gut' hypothesis Figure 3 | The 'leaky gut' hypothesis. a | The normal intestine — an intact barrier, including tight junctions — prevents translocation of bacteria and/or bacterial components or products into the submucosal compartment. b | The 'leaky gut': disruption of tight junction integrity permits bacteria (from a normal or altered gut microbiota) to access the submucosa, where they activate mast cells and lymphocytes that release products such as mast cell proteases and cytokines and chemokines, which lead to inflammation and activation of sensory neurons. Access is also provided to the vasculature and thereby to the portal circulation, the liver and potentially the systemic circulation. As discussed in the main text, this hypothesis is an oversimplification of interactions between the microbiota and the gut barrier, and many of the aforementioned steps have not been demonstrated in humans. Quigley, E. M. M. (2017) Gut microbiome as a clinical tool in gastrointestinal disease management: are we there yet? Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2017.29