Faculty Opinions recommendation of STAT3 deletion during hematopoiesis causes Crohn's disease-like pathogenesis and lethality: a critical role of STAT3 in innate immunity.

2003 ◽  
Author(s):  
Steve Ward
Keyword(s):  
Innate Immunity ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Critical Role

scholarly journals STAT3 deletion during hematopoiesis causes Crohn's disease-like pathogenesis and lethality: A critical role of STAT3 in innate immunity

2003 ◽  
Vol 100 (4) ◽  
pp. 1879-1884 ◽  
Author(s):  
T. Welte ◽  
S. S. M. Zhang ◽  
T. Wang ◽  
Z. Zhang ◽  
D. G. T. Hesslein ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Critical Role

scholarly journals Pathophysiology of Crohn’s disease inflammation and recurrence

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
L. Petagna ◽  
A. Antonelli ◽  
C. Ganini ◽  
V. Bellato ◽  
M. Campanelli ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Innate Immunity ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Surgical Approaches ◽  
Disease Evolution ◽  
Limited Success ◽  
Tnf Α ◽  
Chron's Disease

Abstract Chron’s Disease is a chronic inflammatory intestinal disease, first described at the beginning of the last century. The disease is characterized by the alternation of periods of flares and remissions influenced by a complex pathogenesis in which inflammation plays a key role. Crohn’s disease evolution is mediated by a complex alteration of the inflammatory response which is characterized by alterations of the innate immunity of the intestinal mucosa barrier together with a remodeling of the extracellular matrix through the expression of metalloproteins and increased adhesion molecules expression, such as MAcCAM-1. This reshaped microenvironment enhances leucocytes migration in the sites of inflammation, promoting a TH1 response, through the production of cytokines such as IL-12 and TNF-α. IL-12 itself and IL-23 have been targeted for the medical treatment of CD. Giving the limited success of medical therapies, the treatment of the disease is invariably surgical. This review will highlight the role of inflammation in CD and describe the surgical approaches for the prevention of the almost inevitable recurrence.

Upregulation of TNF-receptor 2 (p80) in Crohn's disease and critical role of p80 in experimental collitis

2001 ◽  
Vol 120 (5) ◽  
pp. A520-A520
Author(s):  
M HOLTMANN ◽  
M SCHUETZ ◽  
P SCHEURICH ◽  
P GALLE ◽  
M NEURATZ
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Critical Role ◽  
Tnf Receptor

Upregulation of TNF-receptor 2 (p80) in Crohn's disease and critical role of p80 in experimental collitis

2001 ◽  
Vol 120 (5) ◽  
pp. A520
Author(s):  
Martin H. Holtmann ◽  
Michael Schuetz ◽  
Peter Scheurich ◽  
Peter R. Galle ◽  
Markus F. Neuratz
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Critical Role ◽  
Tnf Receptor

scholarly journals The Critical Role of LIGHT in Promoting Intestinal Inflammation and Crohn’s Disease

2005 ◽  
Vol 174 (12) ◽  
pp. 8173-8182 ◽  
Author(s):  
Jing Wang ◽  
Robert A. Anders ◽  
Yang Wang ◽  
Jerrold R. Turner ◽  
Clara Abraham ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Intestinal Inflammation ◽  
Critical Role ◽  
Role Of Light

scholarly journals Tsc1 regulates tight junction independent of mTORC1

2021 ◽  
Vol 118 (30) ◽  
pp. e2020891118
Author(s):  
Mingqiang Lai ◽  
Wenchong Zou ◽  
Zelong Han ◽  
Ling Zhou ◽  
Zeyou Qiu ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Tight Junction ◽  
Actin Cytoskeleton ◽  
Critical Role ◽  
Adherens Junction ◽  
Cell Junctions ◽  
Whole Body ◽  
Mechanistic Target Of Rapamycin

Tuberous sclerosis complex 1 (Tsc1) is a tumor suppressor that functions together with Tsc2 to negatively regulate the mechanistic target of rapamycin complex 1 (mTORC1) activity. Here, we show that Tsc1 has a critical role in the tight junction (TJ) formation of epithelium, independent of its role in Tsc2 and mTORC1 regulation. When an epithelial cell establishes contact with neighboring cells, Tsc1, but not Tsc2, migrates from the cytoplasm to junctional membranes, in which it binds myosin 6 to anchor the perijunctional actin cytoskeleton to β-catenin and ZO-1. In its absence, perijunctional actin cytoskeleton fails to form. In mice, intestine-specific or inducible, whole-body Tsc1 ablation disrupts adherens junction/TJ structures in intestine or skin epithelia, respectively, causing Crohn’s disease–like symptoms in the intestine or psoriasis-like phenotypes on the skin. In patients with Crohn’s disease or psoriasis, junctional Tsc1 levels in epithelial tissues are markedly reduced, concomitant with the TJ structure impairment, suggesting that Tsc1 deficiency may underlie TJ-related diseases. These findings establish an essential role of Tsc1 in the formation of cell junctions and underpin its association with TJ-related human diseases.

P056 DISCRIMINATORY ROLE OF ANTI-MICROBIAL ANTIBODIES IN DIAGNOSIS OF CROHN'S DISEASE AGAINST NORMAL AND OTHER MIMICS

2020 ◽  
Vol 158 (3) ◽  
pp. S21-S22
Author(s):  
Peilin Zhang ◽  
Lawrence Minardi ◽  
J. Todd Kuenstner ◽  
Steve Zekan ◽  
Rusty Kruzelock
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease

THE EVALUATION OF SERUM SEROTONIN LEVEL AMONG PATIENTS WITH CROHN’S DISEASE AND ITS IMPACT ON QUALITY OF LIFE

2021 ◽  
Vol 27 (Supplement_1) ◽  
pp. S55-S55
Author(s):  
Marcin Sochal ◽  
Piotr Bialasiewicz ◽  
Agata Gabryelska ◽  
Renata Talar-Wojnarowska ◽  
Jakub Fichna ◽  
...  
Keyword(s):  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Sleep Quality ◽  
Sleep Fragmentation ◽  
Clinical Severity ◽  
Serotonin Level ◽  
Intestinal Physiology ◽  
Tnf Α

Abstract Background and aims Serotonin affects intestinal physiology, mood, as well as circadian rhythm. Moreover, serotonin has proinflammatory function. Therefore, the aim of this study was to investigate the role of serotonin in clinical severity of Crohn’s Disease (CD) and its effect on pain and sleep quality. Methods Fifty-nine CD patients (34 in exacerbation and 25 in remission according to the Harvey-Bradshaw Index-HBI) and 25 health control individuals(HC) were recruited. Sleep quality was assessed by the Pittsburgh Sleep Quality Index (PSQI) and subjective severity of pain by the Visual Analog Scale (VAS). Seventeen patients were treated with anti-TNF-α induction therapy for 14 weeks. Results Serotonin level was higher in CD (145.12ng/mL, IQR:98.14–179.25) compared to HC (87.52ng/mL, IQR:70.04–129.39; p=0.002) and in exacerbation of CD (157.66ng/mL, IQR:111.94–197.64) compared to remission (122.33ng/mL, IQR:83.28–163.67; p=0.029). Serotonin level with cut-off point of 92.45 ng/mL is useful for distinguishing participants with CD from HC (sensitivity: 78%, specificity: 60%, positive predictive value: 82%). Positive correlation between serotonin and HBI (r=0.279, p=0.032) and severity of diarrhoea (r=0.260, p=0.047) were found. Serotonin does not correlate with PSQI (r=0.152, p=0.168), but correlates with presence of sleep fragmentation for example by getting up to use the bathroom (joined 5b-5j PSQI questions; r=0.270, p=0.039). Correlations between serotonin and VAS were also obtained (r=0.220, p=0.045). Moreover, serotonin level significantly decreased after anti-TNF-α therapy (192.35ng/mL, IQR:150.36–225.56 vs. 121.11ng/mL, IQR:91.28–188.87; p=0.006). The study was funded by National Science Centre, Poland (#2018/31/N/NZ5/03715). Conclusions Serotonin level correlates with the severity of CD and decreases after anti-TNF-α therapy. It is associated with sleep fragmentation, which may be caused by diarrhea.

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