scholarly journals Exploratory Investigation of Intestinal Structure and Function after Stroke in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Diya Ye ◽  
Yuting Hu ◽  
Ning Zhu ◽  
Weizhong Gu ◽  
Gao Long ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Intestinal Mucosa ◽  
Caspase 3 ◽  
Disease Model ◽  
Death Receptor ◽  
Intestinal Barrier ◽  
Structure And Function ◽  
Intestinal Barrier Function ◽  
Tnf Α ◽  
And Function

Stroke is the second leading cause of death worldwide. Patients who have a stroke are susceptible to many gastrointestinal (GI) complications, such as dysphagia, GI bleeding, and fecal incontinence. However, there are few studies focusing on the GI tract after stroke. The current study is to investigate the changes of intestinal structure and function in mice after ischemic stroke. Ischemic stroke was made as a disease model in mice, in which brain and ileal tissues were collected for experiments on the 1st and 7th day after stroke. Intestinal motility of mice was inhibited, and intestinal permeability was increased after stroke. Hematoxylin-eosin (HE) staining showed the accumulation of leucocytes in the intestinal mucosa. Myeloperoxidase (MPO) activity and inflammatory proteins (nuclear factor kappa-B (NF-κB), inducible nitric oxide synthase (iNOS)) in the small intestine were significantly increased in mice after stroke. The expression of tight junction (TJ) proteins (zonula occludens-1 (ZO-1), occludin, and claudin-1) was downregulated, and transmission electron microscopy (TEM) showed broken TJ of the intestinal mucosa after stroke. Glial fibrillary acidic protein (GFAP) and the apoptosis-associated proteins (tumor necrosis factor (TNF-α), caspase-3, and cleaved caspase-3) were notably upregulated as well. Ischemic stroke led to negative changes on intestinal structure and function. Inflammatory mediators and TNF-α-induced death receptor signaling pathways may be involved and disrupt the small intestinal barrier function. These results suggest that stroke patients should pay attention to GI protection.

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

2020 ◽  
Vol 8 (11) ◽  
pp. 1744
Author(s):  
Lakshya Sharma ◽  
Antonio Riva
Keyword(s):  
Intestinal Barrier ◽  
Therapeutic Strategies ◽  
Structure And Function ◽  
Intestinal Barrier Function ◽  
Current Evidence ◽  
Barrier Functions ◽  
Microbial Dysbiosis ◽  
Health And Disease ◽  
And Function

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.

15-Lipoxygenase-2 Deficiency Induces a Dysfunction in Macrophages That Can Be Restored by Salidroside

2021 ◽  
Author(s):  
Rong Huang Huang ◽  
Tingting Li Li ◽  
Xi Yong Yong ◽  
Huling Wen Wen ◽  
Xing Zhou Zhou ◽  
...  
Keyword(s):  
Natural Product ◽  
Signaling Pathway ◽  
Therapeutic Strategy ◽  
Caspase 3 ◽  
Mechanisms Of Action ◽  
Rna Seq ◽  
Immunological Function ◽  
Tnf Α ◽  
And Function ◽  
Genetic Strategies

Abstract 15-Lipoxygenase-2(15-LOX-2) is thought to regulate inflammation and immunological function however, its mechanisms of action are still unclear. Furthermore, it has been reported that salidroside has anti inflammatory properties , but its role in macrophage function has not been understood yet In this study, we aimed to determine how 15-LOX-2 expression level s affect the function of macrophages and the effect of salidroside on 15-LOX-2 deficient macrophages We used multiple functional genetic strategies to determine 15-LOX-2 function in macrophages. 15-LOX-2 deficiency promotes phagocytosis and proliferation of macrophages and impairs their apoptosis Mechanistically, t he expression levels of cyclophilinB (CypB) were upregulated in 15-LOX-2 deficient Ana 1 macrophages, whereas those of caspase 3 were down regulated. Furthermore, RNA-seq analysis showed that inflammation, complement, and TNF-α signaling pathway s were all activated in 15-LOX-2 deficient Ana 1 macrophages. Treatment of 15-LOX-2 deficient macrophages with salidroside, a natural product derived from Rhodiola species, effectively reversed the effects of 15-LOX-2 deficiency on caspase 3 and CypB levels, as well as on apoptosis and proliferation. In conclusion, our study shows that there is a newly identified link between 15-LOX-2 deficiency and salidroside in regulating macrophage survival, proliferation, and function. Salidroside may be a promising therapeutic strategy for treating inflammation related diseases resulting from 15-LOX-2 deficiency.

Expression of α-Defensins, CD20+ B-lymphocytes, and Intraepithelial CD3+ T-lymphocytes in the Intestinal Mucosa of Patients with Liver Cirrhosis: Emerging Mediators of Intestinal Barrier Function

2018 ◽  
Vol 63 (10) ◽  
pp. 2582-2592 ◽  
Author(s):  
Georgios I. Tsiaoussis ◽  
Eleni C. Papaioannou ◽  
Eleni P. Kourea ◽  
Stelios F. Assimakopoulos ◽  
Georgios I. Theocharis ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
T Lymphocytes ◽  
B Lymphocytes ◽  
Intestinal Mucosa ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function

Dynamics of enterocyte tight junctions: effect of experimental colitis and two different anti-TNF strategies

2008 ◽  
Vol 294 (4) ◽  
pp. G938-G947 ◽  
Author(s):  
Walter Fries ◽  
Carmelo Muja ◽  
Carmela Crisafulli ◽  
Salvatore Cuzzocrea ◽  
Emanuela Mazzon
Keyword(s):  
Intestinal Barrier ◽  
Experimental Colitis ◽  
Intestinal Barrier Function ◽  
Cell Contact ◽  
Rapid Loss ◽  
Zonula Occludens ◽  
Tnf Α ◽  
Zonula Occludens 1 ◽  
Early Effects ◽  
Present Setting

An alteration of the intestinal barrier is considered to represent an early step in pathogenesis of Crohn's disease. The integrity of intestinal barrier function is guaranteed among other factors by enterocyte tight junction (TJ) proteins. Clinical and experimental data indicate the TNF-α to be the major responsible factor for these defects. In the present study we investigated the very early effects of DNBS-ethanol colitis on ileal enterocyte TJ proteins [occludin, zonula occludens-1 (ZO-1), claudin-2] in controls, mice treated with infliximab (IFX) or with etanercept (ETC), and in knockout mice for the TNF-α receptor 1 (TNFR-1−/−). Circulating TNF-α levels were effectively reduced by IFX and ETC ( P < 0.01, both) at 3 and at 6 h. DNBS colitis induced disappearance of occludin and ZO-1 from enterocyte cell-cell contact, whereas claudin-2, absent under control conditions, appeared in the ileal epithelium. These alterations were prevented equally by both treatments, IFX and ETC, and in TNFR-1−/− animals. DNBS colitis induced a very rapid loss of occludin and ZO-1 from ileal TJ together with an upregulation of claudin-2. Our data are consistent with the hypothesis that TNF-α is involved in early TJ rearrangement and that its effects are mediated through TNFR-1. Despite clinical differences, both anti-TNF treatments were equally effective in the present setting.

scholarly journals Role for diet in normal gut barrier function: developing guidance within the framework of food-labeling regulations

2019 ◽  
Vol 317 (1) ◽  
pp. G17-G39 ◽  
Author(s):  
Michael Camilleri ◽  
Barbara J. Lyle ◽  
Karen L. Madsen ◽  
Justin Sonnenburg ◽  
Kristin Verbeke ◽  
...  
Keyword(s):  
Barrier Function ◽  
Intestinal Barrier ◽  
Normal Function ◽  
Model Systems ◽  
Intestinal Barrier Function ◽  
Dietary Interventions ◽  
Labeling Regulations ◽  
Gut Barrier Function ◽  
And Function

A reduction in intestinal barrier function is currently believed to play an important role in pathogenesis of many diseases, as it facilitates passage of injurious factors such as lipopolysaccharide, peptidoglycan, whole bacteria, and other toxins to traverse the barrier to damage the intestine or enter the portal circulation. Currently available evidence in animal models and in vitro systems has shown that certain dietary interventions can be used to reinforce the intestinal barrier to prevent the development of disease. The relevance of these studies to human health is unknown. Herein, we define the components of the intestinal barrier, review available modalities to assess its structure and function in humans, and review the available evidence in model systems or perturbations in humans that diet can be used to fortify intestinal barrier function. Acknowledging the technical challenges and the present gaps in knowledge, we provide a conceptual framework by which evidence could be developed to support the notion that diet can reinforce human intestinal barrier function to restore normal function and potentially reduce the risk for disease. Such evidence would provide information on the development of healthier diets and serve to provide a framework by which federal agencies such as the US Food and Drug Administration can evaluate evidence linking diet with normal human structure/function claims focused on reducing risk of disease in the general public.

scholarly journals Dietary seaweed-derived polysaccharides improve growth performance of weaned pigs through maintaining intestinal barrier function and modulating gut microbial populations

2020 ◽  
Author(s):  
Tiande Zou ◽  
Jin Yang ◽  
Xiaobo Guo ◽  
Qin He ◽  
Zirui Wang ◽  
...  
Keyword(s):  
Growth Performance ◽  
Intestinal Barrier ◽  
Basal Diet ◽  
Intestinal Barrier Function ◽  
Control Group ◽  
Mrna Levels ◽  
Intestinal Health ◽  
Weaned Pigs ◽  
Tnf Α ◽  
G Ratio

Abstract Background: Seaweed-derived polysaccharides (SDP) represent an attractive source of prebiotic nutraceuticals for the food and animal husbandry industry. However, the mechanism by which SDP from Enteromorpha mediates pig growth are not fully understood. This study aimed to investigate how SDP supplementation influences the growth performance and intestinal health in weaned pigs.Results: In Exp. 1, 240 weaned pigs were randomly assigned to four dietary treatments and fed with a basal diet or a basal diet containing 200, 400 or 800 mg/kg SDP, respectively, in a 21-d trial. Pigs on the 400 or 800 mg/kg SDP-supplemented group had greater ADG and lower F/G ratio than those on the control group (P＜0.05). In Exp. 2, 20 male weaned pigs were randomly assigned to two treatments and fed with a basal diet (CON group) or a basal diet supplemented with 400 mg/kg SDP (the optimum does from Exp. 1), in a 21-d trial. Pigs fed the SDP diet had greater ADG, the concentrations of serum IL-6 and TNF-α and the activities of glutathione peroxidase, superoxide dismutase and catalase (P＜0.05), and lower F/G, diarrhea rate, as well as serum D-lactate concentrations and diamine oxidase activity (P＜0.05). Moreover, dietary SDP supplementation enhanced secretory immunoglobulin A content, villus height and villous height: crypt depth ratio in small intestine, as well as the lactase and maltase activities in jejunum mucosa (P＜0.05). SDP supplementation elevated the mRNA levels of inflammatory response-related genes (IL-6, TNF-α, TLR4, TLR6 and MyD88), and the mRNA and protein levels of ZO-1, Claudin-1 and Occludin in jejunum mucosa (P＜0.05). Importantly, SDP not only increased the Lactobacillus population but also reduced the Escherichia coli population in cecum (P＜0.05). Furthermore, SDP increased acetic acid and butyric acid concentrations in cecum (P＜0.05).Conclusions: These results not only suggest a beneficial effect of SDP on growth performance and intestinal barrier functions, but also offer potential mechanisms behind SDP-facilitated intestinal health in weaned pigs.

scholarly journals Tolerogenic Dendritic Cells Shape a Transmissible Gut Microbiota that Protects from Metabolic Diseases

2021 ◽  
Author(s):  
Emelyne Lécuyer ◽  
Tiphaine Le Roy ◽  
Aurélie Gestin ◽  
Amélie Lacombe ◽  
Catherine Philippe ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Metabolic Diseases ◽  
Intestinal Inflammation ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Low Grade ◽  
Obesity And Diabetes ◽  
Tolerogenic Dendritic Cells ◽  
Tolerogenic Function ◽  
And Function

Excess of chronic contact between microbial motifs and intestinal immune cells are known to trigger a low-grade inflammation involved in many pathologies such as obesity and diabetes. <p>The important skewing of intestinal adaptive immunity in the context of diet-induced obesity (DIO) is well described but how dendritic cells (DCs) participate to these changes is still poorly documented. To address this question, transgenic mice with enhanced DCs lifespan and immunogenicity (DC<sup>hBcl-2</sup> mice) are challenged with a high-fat diet.</p> <p>Those mice display resistance to DIO and metabolic alterations. The DIO-resistant phenotype is associated with healthier parameters of intestinal barrier function and lower intestinal inflammation. DC<sup>hBcl-2</sup> DIO-resistant mice demonstrate a particular increase in tolerogenic DC numbers and function which is associated with strong intestinal IgA, Th17 and T regulatory immune responses.</p> <p>Microbiota composition and function analyses reveal that the DC<sup>hBcl-2</sup> mice microbiota is characterized by lower immunogenicity and an enhanced butyrate production. Cohousing experiments and fecal microbial transplantations are sufficient to transfer the DIO resistance status to WT mice demonstrating that maintenance of DCs tolerogenic ability sustains a microbiota able to drive DIO resistance. DCs tolerogenic function is revealed as a new potent target in metabolic disease management.</p>

scholarly journals Tolerogenic Dendritic Cells Shape a Transmissible Gut Microbiota that Protects from Metabolic Diseases

2020 ◽  
Author(s):  
Emelyne Lécuyer ◽  
Tiphaine Le Roy ◽  
Aurélie Gestin ◽  
Amélie Lacombe ◽  
Catherine Philippe ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Metabolic Diseases ◽  
Intestinal Inflammation ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Low Grade ◽  
Obesity And Diabetes ◽  
Tolerogenic Dendritic Cells ◽  
Tolerogenic Function ◽  
And Function

ABSTRACTExcess of chronic contact between microbial motifs and intestinal immune cells are known to trigger a low-grade inflammation involved in many pathologies such as obesity and diabetes.The important skewing of intestinal adaptive immunity in the context of diet-induced obesity (DIO) is well described but how dendritic cells (DCs) participate to these changes is still poorly documented. To address this question, transgenic mice with enhanced DCs lifespan and immunogenicity (DChBcl-2 mice), are challenged with a high fat diet.Those mice display resistance to DIO and metabolic alterations. The DIO resistant phenotype is associated with healthier parameters of intestinal barrier function and lower intestinal inflammation. DChBcl-2 DIO-resistant mice demonstrate a particular increase in tolerogenic DC numbers and function which is associated with strong intestinal IgA, Th17 and T regulatory immune responses.Microbiota composition and function analyses reveal that the DChBcl-2 mice microbiota is characterized by a lower immunogenicity and an enhanced butyrate production. Cohousing experiments and fecal microbial transplantations are sufficient to transfer the DIO resistance status to WT mice demonstrating that maintenance of DCs tolerogenic ability sustains a microbiota able to drive DIO resistance. DCs tolerogenic function is revealed as a new potent target in metabolic diseases management.

Sign in / Sign up

Export Citation Format

Share Document