The IL-1β-induced increase in intestinal epithelial tight junction (TJ) permeability has been postulated to be an important
mechanism contributing to intestinal inflammation of Crohn’s disease and other inflammatory conditions of the gut
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shared by Nathan Goodyear on 29 Feb 12
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PLoS ONE: Influence of Milk-Feeding Type and Genetic Risk of Developing Coeliac Disease... - 0 views
www.plosone.org/...journal.pone.0030791
celiac disease PROFICEL study dysbiosis intestinal microbiota breast milk
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Mechanism of IL-1β-Induced Increase in Intestinal Epithelial Tight Junction P... - 0 views
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The IL-1β-induced increase in MLCK mRNA transcription and subsequent increase in MLCK protein expression and Caco-2 TJ permeability was mediated by activation of NF-κB
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Anatomical basis of tolerance and immunity to intestinal antigens : Abstract : Nature R... - 0 views
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shared by Nathan Goodyear on 20 Oct 14
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Homeostasis in Intestinal Epithelium Is Orchestrated by the Circadian Clock and Microbi... - 0 views
www.sciencedirect.com/...S0092867413004625
gut microbiota microflora flora intestinal epithelial cells metabolism TLRs MAMPs
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a lack of microbiota results in a permanent ileal overproduction of corticosterone due to decreased expression of the D-box-binding E4BP4 repressor. This hypercorticosterolism generates systemic metabolic defects (hyperglycemia, insulin resistance, increased TG and FA)
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Diet and Herbal Remedies for Ulcerative Colitis - 0 views
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It is an inflammatory, refractory disease which includes colon, rectum and little part of small intestine. The person who is suffering from Ulcerative colitis in tests shows ulcers inside the colon. Ulcerative colitis comes under the category of ...
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It is an inflammatory, refractory disease which includes colon, rectum and little part of small intestine. The person who is suffering from Ulcerative colitis in tests shows ulcers inside the colon. Ulcerative colitis comes under the category of ...
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shared by Nathan Goodyear on 29 Feb 12
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Tight Junctions, Intestinal Permeability, and Autoimmunity Celiac Disease and Type 1 Di... - 0 views
www.ncbi.nlm.nih.gov/...PMC2886850
gut flora microbiota bacteroides bifidobacterium lactobacillus dysbiosis leaky celiac disease diabetes
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shared by Nathan Goodyear on 27 Jul 14
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Diet-Induced Dysbiosis of the Intestinal Microbiota and the Effects on Immunity and Dis... - 0 views
www.ncbi.nlm.nih.gov/...PMC3448089
dysbiosis diet nutrition metabolic endotoxemia disease inflammation gut
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The gut microbiota participates in the body’s metabolism by affecting energy balance, glucose metabolism, and low-grade inflammation associated with obesity and related metabolic disorders
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Firmicutes and Bacteroidetes represent the two largest phyla in the human and mouse microbiota and a shift in the ratio of these phyla has been associated with many disease conditions, including obesity
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there is conflicting evidence on the composition of the obese microbiota phenotype with regards to Bacteroidetes and Firmicutes ratios
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Bifidobacteria spp. from the phyla Actinobacteria, has been shown to be depleted in both obese mice and human subjects
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While it is not yet clear which specific microbes are inducing or preventing obesity, evidence suggests that the microbiota is a factor.
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targeted manipulation of the microbiota results in divergent metabolic outcomes depending on the composition of the diet
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The microbiota has been linked to insulin resistance or type 2 diabetes (T2D) via metabolic syndrome and indeed the microbiota of individuals with T2D is also characterized by an increased Bacteroidetes/Firmicutes ratio, as well as an increase in Bacillus and Lactobacillus spp
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It was also observed that the ratio of Bacteriodes-Prevotella to C. coccoides-E. rectale positively correlated with glucose levels but did not correlate with body mass index [80]. This suggests that the microbiota may influence T2D in conjunction with or independently of obesity
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In humans, high-fat Western-style diets fed to individuals over one month can induce a 71% increase in plasma levels of endotoxins, suggesting that endotoxemia may develop in individuals with GI barrier dyfunction connected to dysbiosis
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LPS increases macrophage infiltration essential for systemic inflammation preceding insulin resistance, LPS alone does not impair glucose metabolism
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early treatment of dysbiosis may slow down or prevent the epidemic of metabolic diseases and hence the corresponding lethal cardiovascular consequences
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increased Firmicutes and decreased Bacteroidetes, which is the microbial profile found in lean phenotypes, along with an increase in Bifidobacteria spp. and Lactobacillus spp
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mouse and rat models of T1D have been shown to have microbiota marked by decreased diversity and decreased Lactobacillus spp., as well as a decrease in the Firmicutes/Bacteroidetes ratio
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The microbiota appears to be essential in maintaining the Th17/Treg cell balance in intestinal tissues, mesenteric and pancreatic lymph nodes, and in developing insulitis, although progression to overt diabetes has not been shown to be controlled by the microbiota
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Lactobacillus johnsonii N6.2 protects BB-rats from T1D by mediating intestinal barrier function and inflammation [101,102] and a combination probiotic VSL#3 has been shown to attenuate insulitis and diabetes in NOD mice
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breast fed infants have higher levels of Bifidobacteria spp. while formula fed infants have higher levels of Bacteroides spp., as well as increased Clostridium coccoides and Lactobacillus spp
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In mice fed a diet high in fat, there are many key gut population changes, such as the absence of gut barrier-protecting Bifidobacteria spp
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diet has a dominating role in shaping gut microbiota and changing key populations may transform healthy gut microbiota into a disease-inducing entity
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“Western” diet, which is high in sugar and fat, causes dysbiosis which affects both host GI tract metabolism and immune homeostasis
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shared by Nathan Goodyear on 07 Sep 11
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The intestine and its microflora are partners for the protection of the host: report on... - 0 views
www.ajcn.org/...675.abstract
microflora probiotics probiotic gut bacteria immune system health intesting
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The intestine is the primary immune organ of the body represented by the gut-associated lymphoid tissue through innate and acquired immunity
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Role of faecal calprotectin as non-invasive marker of intestinal inflammation - 0 views
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shared by Nathan Goodyear on 04 Aug 14
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Metabolic endotoxemia: a molecular link between obesity and cardiovascular risk - 0 views
jme.endocrinology-journals.org/...R51.full
metabolic endotoxemia obesity insulin resistance cardiovascular disease LPS inflammation
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The starting point for innate immunity activation is the recognition of conserved structures of bacteria, viruses, and fungal components through pattern-recognition receptors
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TLRs are transmembrane proteins containing extracellular domains rich in leucine repeat sequences and a cytosolic domain homologous to the IL1 receptor intracellular domain
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The major proinflammatory mediators produced by the TLR4 activation in response to endotoxin (LPS) are TNFα, IL1β and IL6, which are also elevated in obese and insulin-resistant patients
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Obesity, high-fat diet, diabetes, and NAFLD are associated with higher gut permeability leading to metabolic endotoxemia.
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LPS promotes hepatic insulin resistance, hypertriglyceridemia, hepatic triglyceride accumulation, and secretion of pro-inflammatory cytokines promoting the progression of fatty liver disease.
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In the endothelium, LPS induces the expression of pro-inflammatory, chemotactic, and adhesion molecules, which promotes atherosclerosis development and progression.
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In the adipose tissue, LPS induces adipogenesis, insulin resistance, macrophage infiltration, oxidative stress, and release of pro-inflammatory cytokines and chemokines.
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the gut microbiota has been recently proposed to be an environmental factor involved in the control of body weight and energy homeostasis by modulating plasma LPS levels
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dietary fats alone might not be sufficient to cause overweight and obesity, suggesting that a bacterially related factor might be responsible for high-fat diet-induced obesity.
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This was accompanied in high-fat-fed mice by a change in gut microbiota composition, with reduction in Bifidobacterium and Eubacterium spp.
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n humans, it was also shown that meals with high-fat and high-carbohydrate content (fast-food style western diet) were able to decrease bifidobacteria levels and increase intestinal permeability and LPS concentrations
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it was demonstrated that, more than the fat amount, its composition was a critical modulator of ME (Laugerette et al. 2012). Very recently, Mani et al. (2013) demonstrated that LPS concentration was increased by a meal rich in saturated fatty acids (SFA), while decreased after a meal rich in n-3 polyunsaturated fatty acids (n-3 PUFA).
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this effect seems to be due to the fact that some SFA (e.g., lauric and mystiric acids) are part of the lipid-A component of LPS and also to n-3 PUFA's role on reducing LPS potency when substituting SFA in lipid-A
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these experimental results suggest a pivotal role of CD14-mediated TLR4 activation in the development of LPS-mediated nutritional changes.
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This suggests a link between gut microbiota, western diet, and obesity and indicates that gut microbiota manipulation can beneficially affect the host's weight and adiposity.
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endotoxemia was independently associated with energy intake but not fat intake in a multivariate analysis
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in vitro that endotoxemia activates pro-inflammatory cytokine/chemokine production via NFκB and MAPK signaling in preadipocytes and decreased peroxisome proliferator-activated receptor γ activity and insulin responsiveness in adipocytes.
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LPS-induced release of glucagon, GH and cortisol, which inhibit glucose uptake, both peripheral and hepatic
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Recent evidence has been linking ME with dyslipidemia, increased intrahepatic triglycerides, development, and progression of alcoholic and nonalcoholic fatty liver disease
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The hepatocytes, rather than hepatic macrophages, are the cells responsible for its clearance, being ultimately excreted in bile
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All the subclasses of plasma lipoproteins can bind and neutralize the toxic effects of LPS, both in vitro (Eichbaum et al. 1991) and in vivo (Harris et al. 1990), and this phenomenon seems to be dependent on the number of phospholipids in the lipoprotein surface (Levels et al. 2001). LDL seems to be involved in LPS clearance, but this antiatherogenic effect is outweighed by its proatherogenic features
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LPS produces hypertriglyceridemia by several mechanisms, depending on LPS concentration. In animal models, low-dose LPS increases hepatic lipoprotein (such as VLDL) synthesis, whereas high-dose LPS decreases lipoprotein catabolism
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When a dose of LPS similar to that observed in ME was infused in humans, a 2.5-fold increase in endothelial lipase was observed, with consequent reduction in total and HDL. This mechanism may explain low HDL levels in ‘ME’ and other inflammatory conditions such as obesity and metabolic syndrome
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It is known that the high-fat diet and the ‘ME’ increase intrahepatic triglyceride accumulation, thus synergistically contributing to the development and progression of alcoholic and NAFLD, from the initial stages characterized by intrahepatic triglyceride accumulation up to chronic inflammation (nonalcoholic steatohepatitis), fibrosis, and cirrhosis
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On the other hand, LPS activates Kupffer cells leading to an increased production of ROS and pro-inflammatory cytokines like TNFα
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high-fat diet mice presented with ME, which positively and significantly correlated with plasminogen activator inhibitor (PAI-1), IL1, TNFα, STAMP2, NADPHox, MCP-1, and F4/80 (a specific marker of mature macrophages) mRNAs
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prebiotic administration reduces intestinal permeability to LPS in obese mice and is associated with decreased systemic inflammation when compared with controls
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Cani et al. also found that high-fat diet mice presented with not only ME but also higher levels of inflammatory markers, oxidative stress, and macrophage infiltration markers
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This suggests that important links between gut microbiota, ME, inflammation, and oxidative stress are implicated in a high-fat diet situation
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high-fat feeding is associated with adipose tissue macrophage infiltration (F4/80-positive cells) and increased levels of chemokine MCP-1, suggesting a strong link between ME, proinflammatory status, oxidative stress, and, lately, increased CV risk
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markers of systemic inflammation such as circulating bacterial endotoxin were elevated in patients with chronic infections and were strong predictors of increased atherosclerotic risk
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As a TLR4 ligand, LPS has been suggested to induce atherosclerosis development and progression, via a TLR4-mediated inflammatory state.
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shared by fnfdoc on 08 Jun 18
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Symptoms And Causes Of Diverticulitis | Health Blog - 0 views
fnfdoc.com/...symptoms-causes-diverticulitis
Diverticulitis avoid foods Causes Risk Factors Symptoms
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What is diverticulitis and what signs and symptoms occur when you have diverticulitis? What Foods You Should Eat If You Have Diverticulitis and what you should not eat when you discovered you have diverticulitis. Described many causes in this article if you are looking for causes of diverticulitis.
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Diverticulitis is a very serious medical condition. It causes inflamed pouches in the lining of your intestine. It is a very serious medical condition that causes infection or inflammation of small pouches in the lining of your intestine that is known as diverticula that develop along the walls of the intestines.
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shared by Nathan Goodyear on 09 Nov 16
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The role of short-chain fatty acids in the interplay between diet, gut microbiota, and ... - 0 views
www.ncbi.nlm.nih.gov/...PMC3735932
SCFA gut gut health diet nutrition metabolism gut flora gut microbiota
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Acetate, propionate, and butyrate are present in an approximate molar ratio of 60:20:20 in the colon and stool
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SCFAs might play a key role in the prevention and treatment of the metabolic syndrome, bowel disorders, and certain types of cancer
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SCFA administration positively influenced the treatment of ulcerative colitis, Crohn's disease, and antibiotic-associated diarrhea
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Gut bacteria in the cecum and large intestine produce SCFAs mainly from nondigestible carbohydrates that pass the small intestine unaffected
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colonocytes, the first host cells that take up SCFAs and which depend largely on butyrate for their energy supply
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the microbiota act as a metabolic organ that can break down otherwise indigestible food components, degrade potentially toxic food compounds like oxalate, and synthesize certain vitamins and amino acids
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The general idea is that colonocytes prefer butyrate to acetate and propionate, and oxidize it to ketone bodies and CO2
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Exogenous acetate formed by colonic bacterial fermentation enters the blood compartment and is mixed with endogenous acetate released by tissues and organs (103, 104). Up to 70% of the acetate is taken up by the liver (105), where it is not only used as an energy source, but is also used as a substrate for the synthesis of cholesterol and long-chain fatty acids and as a cosubstrate for glutamine and glutamate synthesis
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SCFAs regulate the balance between fatty acid synthesis, fatty acid oxidation, and lipolysis in the body.
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obese animals in this study showed a 50% reduction in relative abundance of the Bacteroidetes (i.e., acetate and propionate producers), whereas the Firmicutes (i.e., butyrate producers) were proportionally increased compared with the lean counterparts.
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In humans the distinct relation between the Firmicutes:Bacteroidetes ratio and obesity is less clear.
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shared by Nathan Goodyear on 01 May 12
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Effects of Polyunsaturated Fatty Acids in Growth Medium on Lipid Composition and on Phy... - 0 views
www.ncbi.nlm.nih.gov/...PMC321255
PUFA poly unsaturated fatty acids GI dysbiosis bacteria microbiota
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Supplementation with Lactobac... [Cell Mol Biol (Noisy-le-grand). 1999] - PubMed - NCBI - 0 views
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Short-term oral exposure to aluminium d - PubMed Mobile - 0 views
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Digestive Diseases and Sciences, Volume 57, Number 5 - SpringerLink - 0 views
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shared by Nathan Goodyear on 18 Jan 12
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Targeting gut microbiota in obesity: effects of prebiotics and probiotics : Article : N... - 0 views
www.nature.com/...nrendo.2011.126.html
LPS lipopolysaccharides gut microbiota dysbiosis inflammation obesity metabolic endotoxemia health probiotics
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Associations between circulating LPS level, consumption of a high-fat diet and the presence of obesity and type 2 diabetes mellitus have been confirmed in humans
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associations have been proposed between high-fat diet, metabolic endotoxemia and levels of inflammatory markers (TLRs and SOCS3) in mononuclear cells
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metabolic endotoxemia is associated with systemic and adipose tissue inflammation in pregnant women with obesity
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A growing amount of evidence indicates that changes in the integrity of the intestinal barrier occur both in the proximal and the distal part of the gut, which can contribute to the entrance of LPS into the systemic circulation
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The low-grade systemic inflammation that characterizes the obese phenotype is controlled by peptides that are produced in the gut. These peptides are influenced by the presence or absence of the gut microbiota
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these findings suggest that the gut microbiota modulates the biological systems that regulate the availability of nutrients, energy storage, fat mass development and inflammation in the host, which are all components of the obese phenotype
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good look of how the the gut health, or lack there of, can influence energy homeostasis and contribute to obesity. This article points to the presence of LPS playing a role in metabolic endotoxemia. It does discuss the importance of the microbiota and their possible role in the low-grade systemic inflammation condition that is obesity.
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