The in vitro anti-inflammatory effects of recombinant anti-CD25 immunotoxin on lamina propria T cells of patients with inflammatory bowel disease are not sufficient to cure experimental colitis in mice

2001 ◽  
Vol 17 (2) ◽  
pp. 77-84 ◽  
Author(s):  
K. Pfister ◽  
B. Wittig ◽  
B. Jüngling ◽  
K. Ecker ◽  
S. Barth ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cells ◽  
Lamina Propria ◽  
Bowel Disease ◽  
Experimental Colitis ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

scholarly journals Food and Food Groups in Inflammatory Bowel Disease (IBD): The Design of the Groningen Anti-Inflammatory Diet (GrAID)

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1067
Author(s):  
Marjo J. E. Campmans-Kuijpers ◽  
Gerard Dijkstra
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Food Group ◽  
Dietary Guidelines ◽  
Current Evidence ◽  
Group Level ◽  
Food Groups ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

Diet plays a pivotal role in the onset and course of inflammatory bowel disease (IBD). Patients are keen to know what to eat to reduce symptoms and flares, but dietary guidelines are lacking. To advice patients, an overview of the current evidence on food (group) level is needed. This narrative review studies the effects of food (groups) on the onset and course of IBD and if not available the effects in healthy subjects or animal and in vitro IBD models. Based on this evidence the Groningen anti-inflammatory diet (GrAID) was designed and compared on food (group) level to other existing IBD diets. Although on several foods conflicting results were found, this review provides patients a good overview. Based on this evidence, the GrAID consists of lean meat, eggs, fish, plain dairy (such as milk, yoghurt, kefir and hard cheeses), fruit, vegetables, legumes, wheat, coffee, tea and honey. Red meat, other dairy products and sugar should be limited. Canned and processed foods, alcohol and sweetened beverages should be avoided. This comprehensive review focuses on anti-inflammatory properties of foods providing IBD patients with the best evidence on which foods they should eat or avoid to reduce flares. This was used to design the GrAID.

scholarly journals DOP53 PTPN2 and TiO2 in the pathogenesis of inflammatory bowel disease

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S092-S092
Author(s):  
J Conde ◽  
M Schwarzfischer ◽  
E Katkeviciute ◽  
J Häfliger ◽  
A Niechcial ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Flow Cytometry ◽  
Titanium Dioxide ◽  
Bowel Disease ◽  
Myeloid Cells ◽  
Food Additive ◽  
Inflammasome Activation ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

Abstract Background Inflammatory bowel disease (IBD) is caused by a complex interaction among genetic, immunological, bacterial and environmental factors. In this scenario, protein tyrosine phosphatase non-receptor type-2 (PTPN2) has been recognised as a risk factor for the development of IBD and functional studies revealed a major role for this protein in the development of experimental colitis through the regulation of the inflammasome, among other processes. In the same way, a potential relationship between diet components and IBD was suggested. In fact, it was reported that the food additive titanium dioxide (TiO2) was able to induce inflammasome activation in vitro and increase colitis severity in vivo. These observations led us to hypothesise a putative relationship between PTPN2 and TiO2 that could explain the effects of this microparticle in the pathogenesis of bowel inflammation. Methods DSS colitis model was performed in mice lacking PTPN2 in myeloid cells and their wild-type littermates, treated or not with titanium dioxide. After that, histology studies, flow cytometry, expression analysis, ELISA and barrier function experiments were performed. Also, bone marrow-derived macrophages (BMDMs) were used for in vitro studies. Results Titanium dioxide was able to exacerbate DSS-induced colitis, especially in mice lacking PTPN2 in myeloid cells. Flow cytometry analysis of the lamina propria revealed significant changes in different immune cell populations such as macrophages. In vitro experiments using BMDMs revealed that TiO2 induced the activation of the inflammasome. Also, this microparticle down-regulated the expression of the anti-inflammatory cytokine IL-10 and these effects were mainly mediated by JNK and ERK kinases. Conclusions The food additive titanium dioxide seems to play a negative role in colitis development by affecting the production of pro- and anti-inflammatory mediators in macrophages. This study reveals a new mechanism by which a certain component of the diet modulates intestinal inflammation.

scholarly journals Defects in CD8+Regulatory T Cells in the Lamina Propria of Patients with Inflammatory Bowel Disease

2005 ◽  
Vol 174 (9) ◽  
pp. 5814-5822 ◽  
Author(s):  
Jens Brimnes ◽  
Matthieu Allez ◽  
Iris Dotan ◽  
Ling Shao ◽  
Atsushi Nakazawa ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cells ◽  
Regulatory T Cells ◽  
Lamina Propria ◽  
Bowel Disease ◽  
Inflammatory Bowel

scholarly journals Multiple Mechanisms of Flaxseed: Effectiveness in Inflammatory Bowel Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Amber Hanif Palla ◽  
Anwar-ul-Hassan Gilani ◽  
Samra Bashir ◽  
Najeeb Ur Rehman
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Periodic Acid ◽  
Phosphodiesterase Inhibitors ◽  
Bactericidal Effect ◽  
Flaxseed Oil ◽  
Periodic Acid Schiff ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

Ethnopharmacological Relevance. Natural products, like Flaxseed (Linum usitatissimum), have traditionally been used in inflammatory bowel disease (IBD). It is known to contain multiple constituents which may account for its effectiveness, as IBD is a multifaceted disease. Aim of the Study. In the current study, we aimed to assess pharmacological basis for the medicinal use of Flaxseed in IBD. Materials and Methods. Aqueous-methanolic crude extracts of Flaxseed (Fs.Cr) and Flaxseed oil were tested against 6% acetic acid- (AA-) induced colitis in BALB/c mice. Microscopic damage parameters of the hematoxylin and eosin-stained and periodic acid-Schiff-alcian blue-stained sections of the colon were scored to be assessed. Possible antispasmodic mechanism was studied on isolated rabbit jejunum, while antibacterial activity was assessed in vitro for microbes implicated in IBD. Results. In AA-induced colitis, Flaxseed oil was found to be more effective in reducing mortality and colonic ulcers than Fs.Cr at 500 mg/kg dose. Fs.Cr was more efficacious in increasing mucin content as compared to oil, exhibiting slightly greater anti-inflammatory effect (50% vs 35%) and reducing depth of lesion (55% vs 42.31%, respectively). Antispasmodic activity of Fs.Cr (0.03 and 0.1 mg/ml) was mediated by phosphodiesterase inhibitors (PDEI, possibly PDE-4 subtype) with a resultant increase in cAMP levels. Flaxseed oil PDEI activity was mild (1 and 3 mg/ml). Fs.Cr (0.1 and 0.3 mg/ml) was potent in exhibiting anticholinergic activity, similar to dicyclomine, whereas Flaxseed oil showed anticholinergic effect at 1 and 3 mg/ml. Flaxseed oil (9 and 14 µg/ml) was bactericidal against enteropathogenic E.coli (EPEC), enterotoxigenic E.coli (ETEC), and enteroaggregative E.coli (EAEC), whereas Fs.Cr exhibited bactericidal effect against EPEC at 100 µg/ml. Conclusions. Results of this study, taken together with previous studies, suggest that Flaxseed possesses anti-inflammatory, antibacterial, and antispasmodic action through multiple pathways and thus offers promising potential to be developed for IBD.

MIP-3α neutralizing monoclonal antibody protects against TNBS-induced colonic injury and inflammation in mice

2007 ◽  
Vol 292 (5) ◽  
pp. G1263-G1271 ◽  
Author(s):  
Kianoosh Katchar ◽  
Ciarán P. Kelly ◽  
Sarah Keates ◽  
Michael J. O'Brien ◽  
Andrew C. Keates
Keyword(s):  
Inflammatory Bowel Disease ◽  
Monoclonal Antibody ◽  
T Cells ◽  
T Cell ◽  
Lamina Propria ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Colonic Injury ◽  
Neutralizing Monoclonal Antibody ◽  
Inflammatory Bowel

A characteristic feature of human inflammatory bowel disease, particularly Crohn's disease, is the presence of activated CD4+T cells. Recently, we have shown that colonic epithelial cell production of macrophage inflammatory protein (MIP)-3α, a CD4 T cell-directed chemokine, is elevated in inflammatory bowel disease. However, the functional relevance of MIP-3α production during intestinal inflammation is poorly understood. The aim of this study was to determine whether MIP-3α production is increased during murine 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis and to examine the effect of anti-MIP-3α neutralizing monoclonal antibody administration in this model. We found that the administration of TNBS significantly increased colonic MIP-3α protein levels in Balb/c mice. Consistent with this, a marked increase in the number of CCR6-bearing lamina propria CD4+and CD8+T cells was also observed in TNBS-treated animals. Treatment of mice with an anti-MIP-3α neutralizing monoclonal antibody significantly reduced TNBS-mediated increases in colonic weight-to-length ratio, mucosal ulceration, histological damage, and myeloperoxidase activity. TNBS-mediated increases in the number of CCR6-bearing lamina propria T cells were also substantially reduced by anti-MIP-3α neutralizing monoclonal antibody treatment. Taken together, our findings indicate that blockade of MIP-3α bioactivity can significantly reduce TNBS-mediated colonic injury and T cell recruitment, suggesting a role for this chemokine in the pathophysiology of intestinal inflammation.

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