scholarly journals Inflammatory Bowel Disease Types Differ in Markers of Inflammation, Gut Barrier and in Specific Anti-Bacterial Response

Cells ◽  
2019 ◽  
Vol 8 (7) ◽  
pp. 719 ◽  
Author(s):  
Stepan Coufal ◽  
Natalie Galanova ◽  
Lukas Bajer ◽  
Zuzana Gajdarova ◽  
Dagmar Schierova ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cell ◽  
Bowel Disease ◽  
Transforming Growth Factor ◽  
T Cell Response ◽  
Gut Barrier ◽  
Markers Of Inflammation ◽  
Gut Barrier Function ◽  
Biomarker Pattern ◽  
Inflammatory Bowel

Crohn’s disease (CD), ulcerative colitis (UC) and inflammatory bowel disease (IBD) associated with primary sclerosing cholangitis (PSC-IBD), share three major pathogenetic mechanisms of inflammatory bowel disease (IBD)-gut dysbiosis, gut barrier failure and immune system dysregulation. While clinical differences among them are well known, the underlying mechanisms are less explored. To gain an insight into the IBD pathogenesis and to find a specific biomarker pattern for each of them, we used protein array, ELISA and flow cytometry to analyze serum biomarkers and specific anti-microbial B and T cell responses to the gut commensals. We found that decrease in matrix metalloproteinase (MMP)-9 and increase in MMP-14 are the strongest factors discriminating IBD patients from healthy subjects and that PSC-IBD patients have higher levels of Mannan-binding lectin, tissue inhibitor of metalloproteinases 1 (TIMP-1), CD14 and osteoprotegerin than patients with UC. Moreover, we found that low transforming growth factor-β1 (TGF-β1) is associated with disease relapse and low osteoprotegerin with anti-tumor necrosis factor-alpha (TNF-α) therapy. Patients with CD have significantly decreased antibody and increased T cell response mainly to genera Eubacterium, Faecalibacterium and Bacteroides. These results stress the importance of the gut barrier function and immune response to commensal bacteria and point at the specific differences in pathogenesis of PSC-IBD, UC and CD.

scholarly journals Effects of Anti-Cytokine Antibodies on Gut Barrier Function

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Fang Liu ◽  
Seul A. Lee ◽  
Stephen M. Riordan ◽  
Li Zhang ◽  
Lixin Zhu
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Barrier Function ◽  
Inflammatory Diseases ◽  
Immunomodulatory Effects ◽  
Gut Barrier ◽  
Barrier Integrity ◽  
Chronic Inflammatory Diseases ◽  
Gut Barrier Function ◽  
Inflammatory Bowel

Anti-cytokine antibodies are used in treating chronic inflammatory diseases and autoimmune diseases such as inflammatory bowel disease and rheumatic diseases. Patients with these diseases often have a compromised gut barrier function, suggesting that anti-cytokine antibodies may contribute to the re-establishment of gut barrier integrity, in addition to their immunomodulatory effects. This paper reviews the effects of anti-cytokine antibodies on gut barrier function and their mechanisms.

The opposing roles of IL-21 and TGFβ1 in chronic inflammatory bowel disease

2011 ◽  
Vol 39 (4) ◽  
pp. 1061-1066 ◽  
Author(s):  
Thomas T. MacDonald ◽  
Iona Bell ◽  
Giovanni Monteleone
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cells ◽  
T Cell ◽  
Cell Survival ◽  
Bowel Disease ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Chronic Inflammatory Bowel Disease ◽  
Inflammatory Bowel ◽  
T Cell Survival

There are large numbers of T-cells in the mucosa of the intestine in healthy individuals. The stimulus for their presence is the normal gut microbiota. For unknown reasons, in patients with IBD (inflammatory bowel disease), there is inappropriate and chronic activation of mucosal T-cells which leads to gut damage and severe morbidity. In one form of IBD, namely Crohn's disease, the T-cells are probably responding to the microbiota. T-cell survival in the gut wall is dependent on pro-inflammatory cytokines and antibody-mediated inhibition of one of these cytokines, TNFα (tumour necrosis factor α), has shown efficacy in patients, thus encouraging investigations of other ways to control mucosal T-cell responses. In the present paper, we give a brief review of T-cell immunology in IBD and then discuss how two particular cytokines, namely IL-21 (interleukin 21), which is generally pro-inflammatory and important in gut T-cell survival and in maintaining Th17 cells, and TGFβ1 (transforming growth factor β1), which is generally immunosuppressive, play opposing roles in gut inflammation.

T cell response to mannans of saccharomyces cerevisiae in inflammatory bowel disease

2000 ◽  
Vol 118 (4) ◽  
pp. A352-A353 ◽  
Author(s):  
Frank Seibold ◽  
Cordula Ruetten ◽  
Michael Scheurlen ◽  
Burkhard Goeke
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Inflammatory Bowel Disease ◽  
T Cell ◽  
Bowel Disease ◽  
Cell Response ◽  
T Cell Response ◽  
Inflammatory Bowel

scholarly journals The T-cell clonal response to SARS-CoV-2 vaccination in inflammatory bowel disease patients is augmented by anti-TNF therapy and often deficient in antibody-responders

2021 ◽  
Author(s):  
Dalin Li ◽  
Alexander Xu ◽  
Emebet Mengesha ◽  
Rebecca Elyanow ◽  
Rachel M. Gittelman ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cell ◽  
Bowel Disease ◽  
T Cell Response ◽  
Antibody Responses ◽  
High Antibody ◽  
Cell Responses ◽  
Vaccine Type ◽  
Inflammatory Bowel ◽  
Antibody Levels

AbstractBackgroundVaccination against SARS-CoV-2 is a highly effective strategy to protect against infection, which is predominantly mediated by vaccine-induced antibodies. Postvaccination antibodies are robustly produced by those with inflammatory bowel disease (IBD) even on immune-modifying therapies but are blunted by anti-TNF therapy. In contrast, T-cell response which primarily determines long-term efficacy against disease progression,, is less well understood. We aimed to assess the post-vaccination T-cell response and its relationship to antibody responses in patients with inflammatory bowel disease (IBD) on immune-modifying therapies.MethodsWe evaluated IBD patients who completed SARS-CoV-2 vaccination using samples collected at four time points (dose 1, dose 2, 2 weeks after dose 2, 8 weeks after dose 2). T-cell clonal analysis was performed by T-cell Receptor (TCR) immunosequencing. The breadth (number of unique sequences to a given protein) and depth (relative abundance of all the unique sequences to a given protein) of the T-cell clonal response were quantified using reference datasets and were compared to antibody responses.ResultsOverall, 303 subjects were included (55% female; 5% with prior COVID) (Table). 53% received BNT262b (Pfizer), 42% mRNA-1273 (Moderna) and 5% Ad26CoV2 (J&J). The Spike-specific clonal response peaked 2 weeks after completion of the vaccine regimen (3- and 5-fold for breadth and depth, respectively); no changes were seen for non-Spike clones, suggesting vaccine specificity. Reduced T-cell clonal depth was associated with chronologic age, male sex, and immunomodulator treatment. It was preserved by non-anti-TNF biologic therapies, and augmented clonal depth was associated with anti-TNF treatment. TCR depth and breadth were associated with vaccine type; after adjusting for age and gender, Ad26CoV2 (J&J) exhibited weaker metrics than mRNA-1273 (Moderna) (p=0.01 for each) or BNT262b (Pfizer) (p=0.056 for depth). Antibody and T-cell responses were only modestly correlated. While those with robust humoral responses also had robust TCR clonal expansion, a substantial fraction of patients with high antibody levels had only a minimal T-cell clonal response.ConclusionAge, sex and select immunotherapies are associated with the T-cell clonal response to SARS-CoV-2 vaccines, and T-cell responses are low in many patients despite high antibody levels. These factors, as well as differences seen by vaccine type may help guide reimmunization vaccine strategy in immune-impaired populations. Further study of the effects of anti-TNF therapy on vaccine responses are warranted.

Characterization of Helicobacter-induced inflammatory bowel disease in IL-10 -/- and T cell deficient mice

2001 ◽  
Vol 120 (5) ◽  
pp. A523-A523
Author(s):  
A BURICH ◽  
R HERSHBERG ◽  
K WAGGIE ◽  
W ZENG ◽  
J VINEY ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cell ◽  
Bowel Disease ◽  
Inflammatory Bowel ◽  
Deficient Mice

GUT-DIRECTED SELF-HYPNOSIS FOR INFLAMMATORY BOWEL DISEASE PROTOCOL: COMPLIMENTARY PSYCHOTHERAPY FOR REMISSION AUGMENTATION, IBS-LIKE SYMPTOMS, AND SURGERY RECOVERY

2021 ◽  
Vol 27 (Supplement_1) ◽  
pp. S53-S53
Author(s):  
Joshua Paulton ◽  
Amanjot Gill ◽  
Joelle Prevost
Keyword(s):  
Inflammatory Bowel Disease ◽  
Stress Response ◽  
Mechanism Of Action ◽  
Bowel Disease ◽  
Relaxation Techniques ◽  
Markers Of Inflammation ◽  
Post Surgery ◽  
Patient Goals ◽  
History Of ◽  
Inflammatory Bowel

Abstract Background Gut-directed hypnosis (GDH) is a complimentary therapy for Inflammatory Bowel Disease (IBD), that can be learnt by patients to practice self-hypnosis. GDH in IBD has augmented remission and improved inflammation. GDH has a history of successful use for Irritable Bowel Syndrome (IBS). In IBD it may also improve IBS-like symptoms in remission and recovery from surgery. GDH is suitable for youth and adult IBD patients. In hypnosis, a relaxed state is inducted then suggestions to subconscious mind processes are made. In IBD, the mechanism of action of GDH is unknown but may influence the disease stress response. Aims Aims are the development of a GDH self-hypnosis protocol for IBD, with appropriate target symptoms. Patients first learn to practice with a clinician, then as complimentary psychotherapy for remission augmentation, IBS-like symptoms, and surgery recovery. Methods GDH is practiced first with a clinician, and then by patients as self-hypnosis (table 1). Patients receive psycho-education on GDH for IBD. Next, appropriate treatment goals are made, based on target symptoms. Relaxation techniques induce patient to a deeply relaxed state. Therapeutic suggestions specific to patient goals are given: verbal suggestions, visualizations, and post-hypnotic suggestions. Suggestions can focus on having a healthy digestive system, inflammation and symptoms reduction, and achievement and sustainment of remission. Patients emerge from hypnosis, are debriefed, and encouraged to practice ongoing self-hypnosis. Results In IBD, GDH self-hypnosis can be learnt from clinicians and practiced by patients as a complimentary therapy. Patients’ achievement and sustainment of remission, with clinical markers of inflammation can be monitored. Patients can monitor subjective improvement of IBS-like symptoms and post surgery, recovery progress can be monitored. Conclusions GDH has a history of use for IBS. In IBD, it has been shown to modulate remission, and may improve IBS-like symptoms, and in surgery recovery. The mechanism of action of GDH in IBD may influence the disease stress response. Clinicians trained in GDH are limited currently. Patients may learn GDH self- hypnosis to as a complimentary psychotherapy.

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