Zinc Supplementation Tightens Leaky Gut in Crohnʼs Disease

El-Tawil, A. M.

doi:10.1002/ibd.21926

Cited by 12 publications

(5 citation statements)

References 5 publications

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“…Increased intestinal mucosal permeability is considered to be a precursor to a variety of intestinal diseases, indicating the possible prerequisite of a dysfunction of intestinal mucosal barrier (Ménard et al, 2010). In recent years, lots of studies have suggested that the pathogenesis of UC and other autoimmune diseases are related to the increase of intestinal mucosal permeability and leaky gut (Hollander, 1999; Fasano, 2012; Sturniolo et al, 2012). Our results indicated that transplantation of fecal suspension had strong inhibition on digestive proteases trypsin and chymotrypsin but increased the activity of fecal β-glucuronidase, which is consistent with our previous study and our hypothesis about the pathogenesis of UC: the decrease of β-glucuronidase activity caused by intestinal flora disorder reduces the conversion of conjugated bilirubin to unconjugated bilirubin in the intestine, leading to impaired inactivation of digestive proteases and damage of intestinal mucosal barrier, increased infiltration of gut bacteria and bacterial toxins into the tissue and blood, which in turn induces a series of immune inflammatory reactions.…”

Section: Discussionmentioning

confidence: 99%

The Functional Role of Fecal Microbiota Transplantation on Dextran Sulfate Sodium-Induced Colitis in Mice

et al. 2019

Front. Cell. Infect. Microbiol.

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Increasingly studies revealed that dysbiosis of gut microbiota plays a pivotal role in the pathogenesis of ulcerative colitis (UC). Fecal microbiota transplantation (FMT) has drawn more and more attention and become an important therapeutic approach. This study aims to examine the facts about the effective components and look into potential mechanisms of FMT. Colitis was induced by 3% (w/v) dextran sulfate sodium (DSS) in drinking water for 7 days. Colitis mice were administered by oral gavage with fecal suspension, fecal supernatant, fecal bacteria, or boiling-killed fecal bacteria from healthy controls and the disease activity index was monitored daily. On the seventh day, mice were euthanized. The length, histological score, parameters related to inflammation, gut barrier functions of the colon, activities of digestive protease and β-glucuronidase in feces were measured. All of the four fecal components showed certain degree of efficacy in DSS-induced colitis, while transplantation of fecal suspension showed the most potent effect as demonstrated by less body weight loss, lower disease activity scores, more expression of tight junction proteins and TRAF6 and IκBα, less expression of TNF-α, IL-1β, IL-10, TLR-4, and MyD88 in gut tissue, as well as restoration of fecal β-glucuronidase and decreases in fecal digestive proteases. These results provide a novel insight into the possible mechanism of FMT and may help to improve and optimize clinical use of FMT.

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Section: Discussionmentioning

confidence: 99%

The Functional Role of Fecal Microbiota Transplantation on Dextran Sulfate Sodium-Induced Colitis in Mice

et al. 2019

Front. Cell. Infect. Microbiol.

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“…Focusing solely on fortifying the gut, there are many nutrients that may strengthen the integrity of the intestinal barrier. For example, Zinc, Vitamin D, and Magnesium are all known to improve the health of the intestinal mucosa lining [201][202][203] . Interestingly, all of these nutrients have been…”

Section: Nutritional Supplementationmentioning

confidence: 99%

The bidirectional gut-brain-microbiota axis as a potential nexus between traumatic brain injury, inflammation, and disease

Sundman

Chen

Subbian

et al. 2017

Brain, Behavior, and Immunity

158

103

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The bidirectional gut-brain-microbiota axis as a potential nexus between traumatic brain injury, inflammation, and disease. AbstractAs head injuries and their sequelae have become an increasingly salient matter of public health, experts in the field have made great progress elucidating the biological processes occurring within the brain at the moment of injury and throughout the recovery thereafter. Given the extraordinary rate at which our collective knowledge of neurotrauma has grown, new insights may be revealed by examining the existing literature across disciplines with a new perspective. This article will aim to expand the scope of this rapidly evolving field of research beyond the confines of the central nervous system (CNS). Specifically, we will examine the extent to which the bidirectional influence of the gut-brain axis modulates the complex biological processes occurring at the time of traumatic brain injury (TBI) and over the days, months, and years that follow. In addition to local enteric signals originating in the gut, it is well accepted that gastrointestinal (GI) physiology is highly regulated by innervation from the CNS. Conversely, emerging data suggests that the function and health of the CNS is modulated by the interaction between 1) neurotransmitters, immune signaling, hormones, and neuropeptides produced in the gut, 2) the composition of the gut microbiota, and 3) integrity of the intestinal wall serving as a barrier to the external environment. Specific to TBI, existing pre-clinical data indicates that head injuries can cause structural and functional damage to the GI tract, but research directly investigating the neuronal consequences of this intestinal damage is lacking. Despite this void, the proposed mechanisms emanating from a damaged gut are closely implicated in the inflammatory processes known to promote neuropathology in the brain following TBI, which suggests the gut-brain axis may be a therapeutic target to reduce the risk of Chronic Traumatic Encephalopathy and other neurodegenerative diseases following TBI. To better appreciate how various peripheral influences are implicated in the health of the CNS following TBI, this paper will also review the secondary biological injury mechanisms and the dynamic pathophysiological response to neurotrauma. Together, this review article will attempt to connect the dots to reveal novel insights into the bidirectional influence of the gut-brain axis and propose a conceptual model relevant to the recovery from TBI and subsequent risk for future neurological conditions.

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“…As zonulin is a major regulator of TJs, a decrease in zonulin concentration is likely to be associated with a decrease in paracellular intestinal permeability. A change in measurements of intestinal permeability was also seen in supplementation with zinc [139], suggesting an improvement in intestinal barrier function; however, the validity of this study and its conclusions have been contested [140].…”

Section: Dietary Treatmentmentioning

confidence: 71%

Intestinal Barrier Function in Health and Disease—Any Role of SARS-CoV-2?

Sharma

Riva

2020

Microorganisms

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Alterations in the structure and function of the intestinal barrier play a role in the pathogenesis of a multitude of diseases. During the recent and ongoing coronavirus disease (COVID-19) pandemic, it has become clear that the gastrointestinal system and the gut barrier may be affected by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, and disruption of barrier functions or intestinal microbial dysbiosis may have an impact on the progression and severity of this new disease. In this review, we aim to provide an overview of current evidence on the involvement of gut alterations in human disease including COVID-19, with a prospective outlook on supportive therapeutic strategies that may be investigated to rescue intestinal barrier functions and possibly facilitate clinical improvement in these patients.

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Zinc Supplementation Tightens Leaky Gut in Crohnʼs Disease

Cited by 12 publications

References 5 publications

The Functional Role of Fecal Microbiota Transplantation on Dextran Sulfate Sodium-Induced Colitis in Mice

The Functional Role of Fecal Microbiota Transplantation on Dextran Sulfate Sodium-Induced Colitis in Mice

The bidirectional gut-brain-microbiota axis as a potential nexus between traumatic brain injury, inflammation, and disease

Intestinal Barrier Function in Health and Disease—Any Role of SARS-CoV-2?

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