scholarly journals P718 Risk of tuberculosis in patients with inflammatory bowel disease receiving biologics using two interferon-γ release assays as monitoring

2019 ◽  
Vol 13 (Supplement_1) ◽  
pp. S480-S481
Author(s):  
R de Francisco ◽  
M Arias-Guillén ◽  
A Castaño-García ◽  
I Pérez-Martínez ◽  
J J Palacios ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Interferon Γ ◽  
Inflammatory Bowel

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 P021 Circulating inflammatory protein and cellular profiles at time of diagnosis classify inflammatory bowel disease patients according to their underlying immune response and clinical disease course

2021 ◽  
Vol 15 (Supplement_1) ◽  
pp. S139-S139
Author(s):  
M Heredia ◽  
M Charrout ◽  
R Klomberg ◽  
M Aardoom ◽  
M Jongsma ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Disease Activity ◽  
Bowel Disease ◽  
Interferon Γ ◽  
Clinical Disease ◽  
Protein Abundance ◽  
Th Cells ◽  
Inflammatory Protein ◽  
Inflammatory Bowel ◽  
Pediatric Ibd

Abstract Background Chronicity of inflammatory bowel disease (IBD) is driven by reactivation of inflammatory memory CD4+ T helper (Th) cells which activate an inflammatory cascade involving innate immune cells and structural intestinal tissue cells. Because of disease heterogeneity, novel treatment strategies tailored to more precisely target the patient’s individual immune defect are required to prevent disease reactivation. We hypothesize that analysis of changes in circulating inflammatory protein abundance combined with phenotyping of circulating Th cells allow to dissect underlying immune pathogenesis and we aim to stratify pediatric IBD patients accordingly. Methods We performed plasma analysis of 92 inflammatory proteins in a cohort of pediatric IBD patients (CD: n=62; UC/IBD-U: n=20), patients with suspicion of IBD but negative diagnosis (n=13) and age-matched healthy controls (HC: n=30). Peripheral blood was obtained at diagnosis and after induction treatment (t=10–14 weeks). Plasma protein concentrations were assessed with Olink Proximity Extension Assay technology® and Th cells were analyzed with flow cytometry. Samples were clustered using hierarchical clustering with Ward linkage. Differential protein abundance was assessed with t-tests at t=0 and a mixed effect model after treatment. Results Thirty-six plasma proteins discriminated pediatric IBD patients from HC. CD and UC/IBD-U patients shared increased abundance of 17 proteins amongst which interleukin-6 and oncostatin-M. Increased abundance of the Th1 cytokine interferon-γ was strictly associated with CD while Th17-associated interleukin-17A was significantly more abundant in UC/IBD-U. Hierarchical clustering of plasma protein profiles discriminated 2 clusters of UC patients with different clinical disease activity and disease extent. In CD, three patient clusters were identified. CD#1 patients had lower clinical disease activity, lower C-reactive protein and higher blood albumin concentrations. Clusters CD#2 and CD#3 had comparable clinical parameters. CD#3 patients had higher abundance of 14 proteins associated with neutrophil function and interferon-γ signaling while CD#2 patients had a marked increase in frequencies of activated (HLA-DR+) memory Th cells. The three CD clusters responded differently to therapy with CD#1 patients exhibiting only a few changes, CD#2 patients showing intermediate modulation and CD#3 patients exhibiting more modulated proteins and greater fold changes. Conclusion Combined plasma immune protein and circulating Th cell profiling discriminates subgroups of pediatric IBD patients during active disease which differ in their response to therapy. Abbreviations: CD: Crohn’s disease; UC: ulcerative colitis; IBD-U: IBD-unclassified.

Altered Expression of Interferon-γ and Interleukin-4 in Inflammatory Bowel Disease

1998 ◽  
Vol 4 (4) ◽  
pp. 285-290 ◽  
Author(s):  
Luisa Camoglio ◽  
Anje A. Te Velde ◽  
Albert J. Tigges ◽  
Pranab K. Das ◽  
Sander J. H. Van Deventer
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Interferon Γ ◽  
Interleukin 4 ◽  
Altered Expression ◽  
Inflammatory Bowel

scholarly journals Characterization of Serum Cytokine Profile in Predominantly Colonic Inflammatory Bowel Disease to Delineate Ulcerative and Crohn's Colitides

2015 ◽  
Vol 8 ◽  
pp. CGast.S20612 ◽  
Author(s):  
Olga Y. Korolkova ◽  
Jeremy N. Myers ◽  
Samuel T. Pellom ◽  
Li Wang ◽  
Amosy E. M'koma
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Current Knowledge ◽  
Univariate Analysis ◽  
Area Under The Curve ◽  
Magnetic Bead ◽  
Interferon Γ ◽  
Serum Cytokine ◽  
Diagnostic Approaches ◽  
Inflammatory Bowel

Background As accessible diagnostic approaches fail to differentiate between ulcerative colitis (UC) and Crohn's colitis (CC) in one-third of patients with predominantly colonic inflammatory bowel disease (IBD), leading to inappropriate therapy, we aim to investigate the serum cytokine levels in these patients in search of molecular biometric markers delineating UC from CC. Methods We measured 38 cytokines, chemokines, and growth factors using magnetic-bead-based multiplex immunoassay in 25 UC patients, 28 CC patients, and 30 controls. Our results are compared with those from a review of current literature regarding advances in serum cytokine profiles and associated challenges preventing their use for diagnostic/prognostic purposes. Results Univariate analysis showed statistically significant increases of eotaxin, GRO, and TNF-α in UC patients compared to controls (Ctrl); interferon γ, interleukin (IL)-6, and IL-7 in CC group compared to Ctrl; and IL-8 in both UC and CC versus Ctrl. No cytokines were found to be different between UC and CC. A generalized linear model identified combinations of cytokines, allowing the identification of UC and CC patients, with area under the curve (AUC) = 0.936, as determined with receiver operating characteristic (ROC) analysis. Conclusions The current knowledge available about circulating cytokines in IBD is often contradictory. The development of an evidence-based tool using cytokines for diagnostic accuracy is still preliminary.

S1731 Differential Regulation of Interleukin-17 and Interferon-γ Production in Inflammatory Bowel Disease

2009 ◽  
Vol 136 (5) ◽  
pp. A-258
Author(s):  
Laura Rovedatti ◽  
Takahiro Kudo ◽  
Paolo Biancheri ◽  
David S. Rampton ◽  
Neel Sengupta ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Interferon Γ ◽  
Differential Regulation ◽  
Interleukin 17 ◽  
Inflammatory Bowel

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.

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