scholarly journals Cannabidiol and palmitoylethanolamide are anti-inflammatory in the acutely inflamed human colon

2017 ◽  
Vol 131 (21) ◽  
pp. 2611-2626 ◽  
Author(s):  
Daniel G. Couch ◽  
Chris Tasker ◽  
Elena Theophilidou ◽  
Jonathan N. Lund ◽  
Saoirse E. O’Sullivan
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Human Colon ◽  
Interferon Γ ◽  
Cytokine Levels ◽  
Drug Treatments ◽  
Inflammatory Bowel ◽  
Anti Inflammatory ◽  
Trpv1 Antagonist ◽  
Factor Α

Objective: We sought to quantify the anti-inflammatory effects of two cannabinoid drugs, cannabidiol (CBD) and palmitoylethanolamide (PEA), in cultured cell lines and compared this effect with experimentally inflamed explant human colonic tissue. These effects were explored in acutely and chronically inflamed colon, using inflammatory bowel disease and appendicitis explants. Design: Caco-2 cells and human colonic explants collected from elective bowel cancer, inflammatory bowel disease (IBD) or acute appendicitis resections, and were treated with the following drug treatments: vehicle, an inflammatory protocol of interferon γ (IFNγ) and tumour necrosis factor α (TNFα; 10 ng/ml), inflammation and PEA (10 µM), inflammation and CBD (10 µM), and PEA or CBD alone, CBD or vehicle were added simultaneously with IFNγ. Nine intracellular signalling phosphoproteins were determined by multiplex. Inflammatory cytokine secretion was determined using ELISA. Receptor mechanisms were investigated using antagonists for CB1, CB2, PPARα, PPARγ, TRPV1 and GPR55. Results: IFNγ and TNFα treatment increased phosphoprotein and cytokine levels in Caco-2 cultures and colonic explants. Phosphoprotein levels were significantly reduced by PEA or CBD in Caco-2 cultures and colonic explants. CBD and PEA prevented increases in cytokine production in explant colon, but not in Caco-2 cells. CBD effects were blocked by the CB2 antagonist AM630 and TRPV1 antagonist SB366791. PEA effects were blocked by the PPARα antagonist GW6471. PEA and CBD were anti-inflammatory in IBD and appendicitis explants. Conclusion: PEA and CBD are anti-inflammatory in the human colon. This effect is not seen in cultured epithelial cells. Appropriately sized clinical trials should assess their efficacy.

scholarly journals Monocyte Chemotactic Protein 1-Induced Protein 1 Is Highly Expressed in Inflammatory Bowel Disease and Negatively Regulates Neutrophil Activities

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Jian Lin ◽  
Gengfeng Li ◽  
Chunjin Xu ◽  
Huiying Lu ◽  
Cui Zhang ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Proinflammatory Cytokines ◽  
Bowel Disease ◽  
Interferon Γ ◽  
Functional Changes ◽  
Monocyte Chemotactic Protein ◽  
Chemotactic Protein ◽  
Inflammatory Bowel ◽  
Factor Α

Monocyte chemotactic protein 1-induced protein 1 (MCPIP-1) is highly expressed in activated immune cells and plays an important role in negatively regulating immune responses. However, its role in regulating neutrophil functions in the pathogenesis of inflammatory bowel disease (IBD) is still unclear. Here, we found that MCPIP-1 was markedly increased at both the transcriptional and translational levels in inflamed mucosa of IBD patients compared with healthy controls, which was mainly expressed in neutrophils. Interestingly, MG-132, a proteasome inhibitor reducing the degradation of MCPIP-1, further facilitated neutrophils to express MCPIP-1 in vitro. Importantly, MCPIP-1 markedly downregulated the production of ROS, MPO, and proinflammatory cytokines (e.g., interleukin-1β, interleukin-6, tumor necrosis factor-α, interleukin-8, and interferon-γ) and suppressed the migration of IBD neutrophils. Consistently, the same functional changes were observed in neutrophils from mice with myeloid-targeted overexpression of MCPIP-1 as MG-132 did. Altogether, these findings suggest that MCPIP-1 plays a negative role in regulating neutrophil activities through suppressing the production of ROS, MPO, and proinflammatory cytokines and inhibiting the migration. MG-132 may partially modulate the function of neutrophils via the induction of MCPIP-1. Therefore, targeting MCPIP-1 or exogenous supplementation of MG-132 may provide a therapeutic approach in the treatment of IBD.

scholarly journals Plasma Osteopontin Predicts Inflammatory Bowel Disease Activities

2015 ◽  
Vol 100 (1) ◽  
pp. 38-43 ◽  
Author(s):  
Shihoko Komine-Aizawa ◽  
Hideki Masuda ◽  
Takerou Mazaki ◽  
Motomi Shiono ◽  
Satoshi Hayakawa ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Inflammatory Diseases ◽  
Interferon Γ ◽  
Clinical Activity ◽  
Colon And Rectum ◽  
Inflammatory Bowel ◽  
Macrophage Colony ◽  
Factor Α ◽  
Normal Controls

Abstract A glycoprotein osteopontin (OPN) is involved in inflammatory diseases, but its roles in inflammatory bowel disease (IBD) are controversial. To analyze the involvement of the systemic immune response, we simultaneously examined plasma OPN levels and 17 cytokines. This study included 24 ulcerative colitis (UC) patients, 17 Crohn's disease (CD) patients, and 23 normal controls. Clinical parameters were also examined. The plasma OPN levels of the UC and CD patients were significantly higher than those of the normal controls and correlated significantly with their clinical activity indices. In the UC patients, significant relationships were observed between the levels of plasma OPN and multiple cytokines, including interleukin (IL) −1β, IL-4, IL-5, IL-6, IL-7, IL-13, interferon-γ, tumor necrosis factor-α, and granulocyte-macrophage colony-stimulating factor. In the CD patients, the correlation was not significant except for IL-8. Our findings reflect different inflammatory states of the colon and rectum in both diseases.

scholarly journals A156 SERUM TUMOUR NECROSIS FACTOR-α ANTAGONIST DRUG CONCENTRATIONS IN PATIENTS WITH PYODERMA GANGRENOSUM ASSOSCIATED WITH INFLAMMATORY BOWEL DISEASE

2021 ◽  
Vol 4 (Supplement_1) ◽  
pp. 162-163
Author(s):  
M Mikail ◽  
A Wilson
Keyword(s):  
Inflammatory Bowel Disease ◽  
Pyoderma Gangrenosum ◽  
Bowel Disease ◽  
Complete Resolution ◽  
Therapeutic Drug ◽  
Drug Concentrations ◽  
Median Serum ◽  
Inflammatory Bowel ◽  
Factor Α ◽  
Necrosis Factor

Abstract Background The utility of therapeutic drug monitoring for guiding the dosing of tumor necrosis factor-α antagonists (TNFAs) in luminal inflammatory bowel disease (IBD) is well-established and well-accepted. TNFAs, specifically infliximab and adalimumab, have become integral to the management of the rare, neutrophilic dermatosis, pyoderma gangrenosum (PG) in IBD. Little is known regarding the target serum TNFA concentrations to guide dosing to achieve resolution of PG in IBD. Aims To describe the serum TNFA concentrations (infliximab or adalimumab) associated with the resolution of PG lesions in patients with IBD. Methods Patients with IBD and associated PG treated with one of infliximab or adalimumab (collectively known as TNFAs) seen at two academic hospitals affiliated with Western University were identified. Serum TNFA concentrations were assessed at the time of PG treatment. Results Nine patients were identified. All patients had IBD-associated PG. Seven patients were treated with infliximab and 2 patients were treated with adalimumab. All patients received standard dosing. Eight patients had complete resolution of their PG, while one had near complete resolution at the time of last follow-up. A median serum infliximab concentration of 3.00 (IQR, 3.52) µg/ml at week 14 and a median serum adalimumab concentration of 2.02 (IQR, 0.98) µg/ml at week 12 were seen at the time of PG treatment. Conclusions Herein, we report low serum TNFA concentrations despite PG healing in a cohort of IBD patients. This is lower than what is in patients for successful TNFA treatment in luminal and fistulising IBD. Funding Agencies NoneNone.

Preparation, characterization, and in vivo evaluation of anti-inflammatory activities of selenium nanoparticles synthesized by Kluyveromyces lactis GG799

2021 ◽  
Author(s):  
Xiao fan Song ◽  
Lei Qiao ◽  
Shuqi Yan ◽  
Yue Chen ◽  
Xina Dou ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Kluyveromyces Lactis ◽  
Selenium Nanoparticles ◽  
Human Diseases ◽  
In Vivo Evaluation ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

Selenium (Se) as an essential micronutrient that has implications in human diseases, including inflammatory bowel disease (IBD), especially with respect to Se deficiencies. Recently, selenium nanoparticles (SeNPs) have attracted significant...

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.

P044 HIF1A IS A SWITCH IN THE PRO- VS ANTI-INFLAMMATORY FOXP3 GENE CIRCUITRY NETWORKS IMPLICATED IN INFLAMMATORY BOWEL DISEASE

2018 ◽  
Vol 24 (suppl_1) ◽  
pp. S15-S16
Author(s):  
Olga F Sarmento ◽  
Phyllis A Svingen ◽  
Mary R Sagstetter ◽  
Michelle M Gonzalez ◽  
Adebowale O Bamidele ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Foxp3 Gene ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

scholarly journals Can We Target Endogenous Anti-inflammatory Responses as a Therapeutic Strategy for Inflammatory Bowel Disease?

2018 ◽  
Vol 24 (10) ◽  
pp. 2123-2134 ◽  
Author(s):  
Ross John Porter ◽  
Caroline Andrews ◽  
Daniel Paul Brice ◽  
Scott Kenneth Durum ◽  
Mairi Hall McLean
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Therapeutic Strategy ◽  
Inflammatory Responses ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

A moderately elevated soy protein diet mitigates inflammatory changes in gut and in bone turnover during chronic TNBS-induced inflammatory bowel disease

2019 ◽  
Vol 44 (6) ◽  
pp. 595-605 ◽  
Author(s):  
Corinne E. Metzger ◽  
S. Anand Narayanan ◽  
David C. Zawieja ◽  
Susan A. Bloomfield
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bone Turnover ◽  
Soy Protein ◽  
Bowel Disease ◽  
Protein Diet ◽  
Trinitrobenzene Sulfonic Acid ◽  
Inflammatory Bowel ◽  
Anti Inflammatory ◽  
The Impact ◽  
Colitis Model

Inflammatory bowel disease is a condition that leads to gut pathologies such as abnormal lymphatic architecture, as well as to systemic comorbidities such as bone loss. Furthermore, current therapies are limited to low efficacy and incur side effects. Dietary interventions have been explored minimally, but may provide a treatment for improving gut outcomes and comorbidities. Indeed, plant-based soy protein has been shown to exert anti-inflammatory effects. Here, we tested the impact of a moderately elevated soy protein diet in a chronic, 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis model on gut and bone inflammatory-mediated pathophysiological adaptations. Colitis was induced by intrarectal administration of TNBS. Gut histopathology was scored, and lymphatic structural changes and the local inflammatory state were assessed via immunofluorescence. In addition, the effects of gut inflammation on bone turnover and osteocyte proteins were determined via histomorphometry and immunohistochemistry, respectively. The moderately elevated soy protein diet produced improvements in both colonic and bone tissues. In TNBS animals given the soy protein intervention, colon histological scores were reduced and the abnormal lymphatic architecture resolved. There were also improvements in bone formation and reduced bone resorption. In addition, TNBS increased inflammatory cytokines such as tumor necrosis factor-α and receptor activator of nuclear factor κ-B ligand in the gut and bone, but this was resolved in both tissues with the dietary soy protein intervention. The moderately elevated soy protein diet mitigated gut and bone inflammation in a chronic, TNBS-induced colitis model, demonstrating the potential for soy protein as a potential anti-inflammatory dietary intervention for inflammatory bowel disease.

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