Role of damage to intestinal barrier in development of psoriasis

2021 ◽  
pp. 34-37
Author(s):  
I. N. Ekimov ◽  
O. V. Pravdina
Keyword(s):  
Intestinal Permeability ◽  
Intestinal Microbiota ◽  
Ussing Chamber ◽  
Intestinal Barrier ◽  
Intestinal Bacteria ◽  
Intestinal Wall ◽  
Diagnostic Significance ◽  
Fatty Acid Binding ◽  
Barrier Permeability

Disorders of interstitial barrier permeability as one of the promising mechanisms of psoriasis formation and development is a trend of the last decades. In the analysis of modern works devoted to the evaluation of the role of intestinal barrier damage in the development of psoriasis, several ways of assessing intestinal permeability have been noted (including measurement of transepithelial electrical responses using a Ussing chamber, measurement of excretion of orally injected molecules, determination of dynamics and kinetics of LPS intestinal bacteria, immunohistochemical confocal analysis of uniform Z-sections perpendicular to the epithelial cell surface, etc.). However, most authors emphasize the diagnostic significance and availability of biomarker detection. Among the described biomarkers, claudin-3, fecal zonulin, α1-antitrypsin, calprotectin and intestinal fatty acid binding protein (I-FABP) are the most valuable. Through these methods of assessing intestinal permeability and the results of their studies, a number of authors practically prove the correlation between the violation of the intestinal microbiota, intestinal barrier permeability and the development of psoriasis, as well as its severity. This aspect is promising to the therapy of patients with psoriasis, which includes correction of intestinal microbiota and intestinal wall permeability.

scholarly journals Role of the Intestinal Microbiome, Intestinal Barrier and Psychobiotics in Depression

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 927
Author(s):  
Paulina Trzeciak ◽  
Mariola Herbet
Keyword(s):  
Immune System ◽  
Intestinal Microbiota ◽  
Intestinal Barrier ◽  
Intestinal Bacteria ◽  
Intestinal Microbiome ◽  
Stress Reactions ◽  
Treatment Of Depression ◽  
Increased Activity ◽  
Excessive Activation

The intestinal microbiota plays an important role in the pathophysiology of depression. As determined, the microbiota influences the shaping and modulation of the functioning of the gut–brain axis. The intestinal microbiota has a significant impact on processes related to neurotransmitter synthesis, the myelination of neurons in the prefrontal cortex, and is also involved in the development of the amygdala and hippocampus. Intestinal bacteria are also a source of vitamins, the deficiency of which is believed to be related to the response to antidepressant therapy and may lead to exacerbation of depressive symptoms. Additionally, it is known that, in periods of excessive activation of stress reactions, the immune system also plays an important role, negatively affecting the tightness of the intestinal barrier and intestinal microflora. In this review, we have summarized the role of the gut microbiota, its metabolites, and diet in susceptibility to depression. We also describe abnormalities in the functioning of the intestinal barrier caused by increased activity of the immune system in response to stressors. Moreover, the presented study discusses the role of psychobiotics in the prevention and treatment of depression through their influence on the intestinal barrier, immune processes, and functioning of the nervous system.

scholarly journals Sauna dehydration as a new physiological challenge model for intestinal barrier function

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Maria Fernanda Roca Rubio ◽  
Ulrika Eriksson ◽  
Robert J. Brummer ◽  
Julia König
Keyword(s):  
Fatty Acid ◽  
Intestinal Permeability ◽  
Barrier Function ◽  
Fatty Acid Binding Protein ◽  
Binding Protein ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Fatty Acid Binding ◽  
Acid Binding Protein

AbstractThe intestinal barrier plays a crucial role in maintaining gut health, and an increased permeability has been linked to several intestinal and extra-intestinal disorders. There is an increasing demand for interventions aimed at strengthening this barrier and for in vivo challenge models to assess their efficiency. This study investigated the effect of sauna-induced dehydration on intestinal barrier function (clinicaltrials.gov: NCT03620825). Twenty healthy subjects underwent three conditions in random order: (1) Sauna dehydration (loss of 3% body weight), (2) non-steroidal anti-inflammatory drug (NSAID) intake, (3) negative control. Intestinal permeability was assessed by a multi-sugar urinary recovery test, while intestinal damage, bacterial translocation and cytokines were assessed by plasma markers. The sauna dehydration protocol resulted in an increase in gastroduodenal and small intestinal permeability. Presumably, this increase occurred without substantial damage to the enterocytes as plasma intestinal fatty acid-binding protein (I-FABP) and liver fatty acid-binding protein (L-FABP) were not affected. In addition, we observed significant increases in levels of lipopolysaccharide-binding protein (LBP), IL-6 and IL-8, while sCD14, IL-10, IFN-ɣ and TNF-α were not affected. These results suggest that sauna dehydration increased intestinal permeability and could be applied as a new physiological in vivo challenge model for intestinal barrier function.

Zonulin: physiological and clinical role in the perinatal period

2020 ◽  
Vol 19 (5) ◽  
pp. 132-139
Author(s):  
A.I. Khavkin ◽  
◽  
N.M. Bogdanova ◽  
V.P. Novikova ◽  
D.V. Yudina ◽  
...  
Keyword(s):  
Intestinal Barrier ◽  
Gastrointestinal Hormones ◽  
Biological Rhythms ◽  
Perinatal Period ◽  
Intestinal Wall ◽  
Normal Functioning ◽  
Clinical Role ◽  
Wall Permeability ◽  
Intercellular Connections

Lifestyle change, including diet changes, often lead to an impairment of biological rhythms regulating production of gastrointestinal hormones, enzymes, neuropeptides, and various cytokines that ensure proper functioning of the digestive tract. Such changes are almost always associated with microbiota disorders and increase permeability of the intestinal mucosa. Zonulin is a diagnostic marker regulating intestinal wall stability and modulating the density of intercellular connections. Its biological role and mechanism of action are being actively studied now. This literature review aims to summarize the results of latest studies published over the last five years analyzing the role of zonulin in various diseases and conditions. The article also covers some aspects suggesting that zonulin can be used as a marker of normal functioning of the intestinal barrier not only in therapeutic, but also in obstetric and pediatric practice. Key words: biomarker, inflammatory cytokines, gestation, depression, zonulin, intestinal barrier, metabolism, microbiota, intestinal wall permeability

Extra-articular manifestations: inflammatory bowel disease

2016 ◽  
Author(s):  
Dirk Elewaut ◽  
Heleen Cypers ◽  
Matthew L. Stoll ◽  
Charles O. Elson
Keyword(s):  
Inflammatory Bowel Disease ◽  
Intestinal Microbiota ◽  
Bowel Disease ◽  
Intestinal Barrier ◽  
Innate Immune ◽  
Intestinal Barrier Function ◽  
Innate Immune Responses ◽  
Susceptible Host ◽  
Inflammatory Bowel

A significant overlap exists between spondyloarthritis (SpA) and inflammatory bowel disease (IBD), particularly in the IL-23/IL-17 pathway. Shared immunologic mechanisms include aberrant innate immune responses, an excess of Th1/Th17-mediated immunity, and inadequate immune regulation. Many genetic factors associated with IBD are involved in host–pathogen interactions and intestinal barrier function, and the intestinal microbiota do appear to play an important role in disease development. Hence the current hypothesis for IBD pathogenesis is that it stems from a dysregulated immune response to intestinal microbiota in a genetically susceptible host. In SpA, evidence for a role of intestinal microbiota is less abundant, but given the overlap with IBD, it is plausible that gut microbiota are important players in SpA pathogenesis as well. However, there are significant genetic differences between these two conditions, as well as differing responses to biologic therapy.

scholarly journals Intestinal Permeability in Children with Celiac Disease after the Administration of Oligofructose-Enriched Inulin into a Gluten-Free Diet—Results of a Randomized, Placebo-Controlled, Pilot Trial

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1736 ◽  
Author(s):  
Natalia Drabińska ◽  
Urszula Krupa-Kozak ◽  
Elżbieta Jarocka-Cyrta
Keyword(s):  
Celiac Disease ◽  
Intestinal Permeability ◽  
Pilot Trial ◽  
Intestinal Barrier ◽  
Substantial Effect ◽  
Gluten Free Diet ◽  
Gluten Free ◽  
Epithelial Surface ◽  
Fatty Acid Binding ◽  
Sugar Absorption

Abnormalities in the intestinal barrier are a possible cause of celiac disease (CD) development. In animal studies, the positive effect of prebiotics on the improvement of gut barrier parameters has been observed, but the results of human studies to date remain inconsistent. Therefore, this study aimed to evaluate the effect of twelve-week supplementation of a gluten-free diet (GFD) with prebiotic oligofructose-enriched inulin (10 g per day) on the intestinal permeability in children with CD treated with a GFD. A pilot, randomized, placebo-controlled nutritional intervention was conducted in 34 children with CD, being on a strict GFD. Sugar absorption test (SAT) and the concentrations of intestinal permeability markers, such as zonulin, intestinal fatty acid-binding protein, claudin-3, calprotectin, and glucagon-like peptide-2, were measured. We found that the supplementation with prebiotic did not have a substantial effect on barrier integrity. Prebiotic intake increased excretion of mannitol, which may suggest an increase in the epithelial surface. Most children in our study seem to have normal values for intestinal permeability tests before the intervention. For individuals with elevated values, improvement in calprotectin and SAT was observed after the prebiotic intake. This preliminary study suggests that prebiotics may have an impact on the intestinal barrier, but it requires confirmation in studies with more subjects with ongoing leaky gut.

scholarly journals Neutralization of interleukin-17A alleviates burn-induced intestinal barrier disruption via reducing pro-inflammatory cytokines in a mouse model

2019 ◽  
Vol 7 ◽  
Author(s):  
Yajun Song ◽  
Yang Li ◽  
Ya Xiao ◽  
Wengang Hu ◽  
Xu Wang ◽  
...  
Keyword(s):  
Intestinal Permeability ◽  
Inflammatory Cytokines ◽  
Intestinal Mucosa ◽  
Intestinal Barrier ◽  
Barrier Disruption ◽  
Zonula Occludens ◽  
Interleukin 17A ◽  
Zonula Occludens 1 ◽  
Pro Inflammatory Cytokines

Abstract Background The intestinal barrier integrity can be disrupted due to burn injury, which is responsible for local and systemic inflammatory responses. Anti-inflammation strategy is one of the proposed therapeutic approaches to control inflammatory cascade at an early stage. Interleukin-17A (IL-17A) plays a critical role in inflammatory diseases. However, the role of IL-17A in the progression of burn-induced intestinal inflammation is poorly understood. In this study, we aimed to investigate the effect of IL-17A and associated pro-inflammatory cytokines that were deeply involved in the pathogenesis of burn-induced intestinal inflammatory injury, and furthermore, we sought to determine the early source of IL-17A in the intestine. Methods Mouse burn model was successfully established with infliction of 30% total body surface area scald burn. The histopathological manifestation, intestinal permeability, zonula occludens-1 expression, pro-inflammatory cytokines were determined with or without IL-17A-neutralization. Flow cytometry was used to detect the major source of IL-17A+ cells in the intestine. Results Burn caused intestinal barrier damage, increase of intestinal permeability, alteration of zonula occludens-1 expressions, elevation of IL-17A, IL-6, IL-1β and tumor necrosis factor-α (TNF-α), whereas IL-17A neutralization dramatically alleviated burn-induced intestinal barrier disruption, maintained zonula occludens-1 expression, and noticeably, inhibited pro-inflammatory cytokines elevation. In addition, we observed that the proportion of intestinal IL-17A+Vγ4+ T subtype cells (but not IL-17A+Vγ1+ T subtype cells) were increased in burn group, and neutralization of IL-17A suppressed this increase. Conclusions The main original findings of this study are intestinal mucosa barrier is disrupted after burn through affecting the expression of pro-inflammatory cytokines, and a protective role of IL-17A neutralization for intestinal mucosa barrier is determined. Furthermore, Vγ4+ T cells are identified as the major early producers of IL-17A that orchestrate an inflammatory response in the burn model. These data suggest that IL-17A blockage may provide a unique target for therapeutic intervention to treat intestinal insult after burn.

scholarly journals Gut Microbiome, Intestinal Permeability, and Tissue Bacteria in Metabolic Disease: Perpetrators or Bystanders?

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1082 ◽  
Author(s):  
Rima M. Chakaroun ◽  
Lucas Massier ◽  
Peter Kovacs
Keyword(s):  
Metabolic Disease ◽  
Intestinal Permeability ◽  
Systemic Inflammation ◽  
Gut Microbiome ◽  
Metabolic Diseases ◽  
Treatment Strategies ◽  
Intestinal Barrier ◽  
Intestinal Bacteria ◽  
Current Evidence ◽  
Microbial Culture

The emerging evidence on the interconnectedness between the gut microbiome and host metabolism has led to a paradigm shift in the study of metabolic diseases such as obesity and type 2 diabetes with implications on both underlying pathophysiology and potential treatment. Mounting preclinical and clinical evidence of gut microbiota shifts, increased intestinal permeability in metabolic disease, and the critical positioning of the intestinal barrier at the interface between environment and internal milieu have led to the rekindling of the “leaky gut” concept. Although increased circulation of surrogate markers and directly measurable intestinal permeability have been linked to increased systemic inflammation in metabolic disease, mechanistic models behind this phenomenon are underdeveloped. Given repeated observations of microorganisms in several tissues with congruent phylogenetic findings, we review current evidence on these unanticipated niches, focusing specifically on the interaction between gut permeability and intestinal as well as extra-intestinal bacteria and their joint contributions to systemic inflammation and metabolism. We further address limitations of current studies and suggest strategies drawing on standard techniques for permeability measurement, recent advancements in microbial culture independent techniques and computational methodologies to robustly develop these concepts, which may be of considerable value for the development of prevention and treatment strategies.

scholarly journals The Role of Intestinal Permeability in Gastrointestinal Disorders and Current Methods of Evaluation

2021 ◽  
Vol 8 ◽  
Author(s):  
Tim Vanuytsel ◽  
Jan Tack ◽  
Ricard Farre
Keyword(s):  
Intestinal Permeability ◽  
Barrier Function ◽  
Crucial Role ◽  
Intestinal Barrier Function ◽  
Current Evidence ◽  
Gastrointestinal Disorders ◽  
Fatty Acid Binding ◽  
Ussing Chambers

An increased intestinal permeability has been described in various gastrointestinal and non-gastrointestinal disorders. Nevertheless, the concept and definition of intestinal permeability is relatively broad and includes not only an altered paracellular route, regulated by tight junction proteins, but also the transcellular route involving membrane transporters and channels, and endocytic mechanisms. Paracellular intestinal permeability can be assessed in vivo by using different molecules (e.g., sugars, polyethylene glycols, 51Cr-EDTA) and ex vivo in Ussing chambers combining electrophysiology and probes of different molecular sizes. The latter is still the gold standard technique for assessing the epithelial barrier function, whereas in vivo techniques, including putative blood biomarkers such as intestinal fatty acid-binding protein and zonulin, are broadly used despite limitations. In the second part of the review, the current evidence of the role of impaired barrier function in the pathophysiology of selected gastrointestinal and liver diseases is discussed. Celiac disease is one of the conditions with the best evidence for impaired barrier function playing a crucial role with zonulin as its proposed regulator. Increased permeability is clearly present in inflammatory bowel disease, but the question of whether this is a primary event or a consequence of inflammation remains unsolved. The gut-liver axis with a crucial role in impaired intestinal barrier function is increasingly recognized in chronic alcoholic and metabolic liver disease. Finally, the current evidence does not support an important role for increased permeability in bile acid diarrhea.

scholarly journals Tight joints and zonulin in the formation of oral tolerance and food allergy

2019 ◽  
pp. 5-9
Author(s):  
N. G. Prikhodchenko ◽  
T. A. Shumatova ◽  
L. A. Grigoryan ◽  
A. V. Gordeets
Keyword(s):  
Food Allergy ◽  
Intestinal Permeability ◽  
Oral Tolerance ◽  
Intestinal Barrier ◽  
Molecular Entity ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Pathological Conditions ◽  
Diagnostic Criterion

Summary: The study represents a review of publications covering molecular entity of intestinal permeability and changes causing its disorders. The current concepts on intestinal barrier, tight joints (TJ) and intestinal permeability under normal and pathological conditions are covered. Special attention has been given to molecular unions of tight joints; a role of dysregulation of the components of the TJ complex in the formation of oral tolerance and food allergy is disclosed. It is shown that the assessment of the intestinal epithelial barrier condition can be a significant diagnostic criterion to control the disease and to assess the effectiveness of treatment.

scholarly journals Microbiome and Gluten

2015 ◽  
Vol 67 (Suppl. 2) ◽  
pp. 27-42 ◽  
Author(s):  
Yolanda Sanz
Keyword(s):  
Environmental Factors ◽  
Intestinal Microbiota ◽  
Disease Onset ◽  
Intestinal Bacteria ◽  
Epidemiological Studies ◽  
Experimental Models ◽  
Healthy Infants ◽  
Hla Dq ◽  
Environmental Trigger

Celiac disease (CD) is a frequent chronic inflammatory enteropathy caused by gluten in genetically predisposed individuals that carry disease susceptibility genes (HLA-DQ2/8). These genes are present in about 30-40% of the general population, but only a small percentage of carriers develops CD. Gluten is the key environmental trigger of CD, but its intake does not fully explain disease onset; indeed, an increased number of cases experience gluten intolerance in late adulthood after many years of gluten exposure. Consequently, additional environmental factors seem to be involved in CD. Epidemiological studies indicate that common perinatal and early postnatal factors influence both CD risk and intestinal microbiota structure. Prospective studies in healthy infants at risk of developing CD also reveal that the HLA-DQ genotype, in conjunction with other environmental factors, influences the microbiota composition. Furthermore, CD patients have imbalances in the intestinal microbiota (dysbiosis), which are not fully normalized despite their adherence to a gluten-free diet. Therefore, it is hypothesized that the disease can promote dysbiosis that aggravates CD pathogenesis, and dysbiosis, in turn, can initiate and sustain inflammation through the expansion of proinflammatory pathobionts and decline of anti-inflammatory mutualistic bacteria. Studies in experimental models are also contributing to understand the role of intestinal bacteria and its interactions with a predisposed genotype in promoting CD. Advances in this area could aid in the development of microbiome-informed intervention strategies that optimize the partnership between the gut microbiota and host immunity for improving CD management.

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