Cytokines in canine inflammatory bowel disease

2013 ◽  
Vol 16 (1) ◽  
pp. 165-171 ◽  
Author(s):  
A. Kołodziejska-Sawerska ◽  
A. Rychlik ◽  
A. Depta ◽  
M. Wdowiak ◽  
M. Nowicki ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Mrna Expression ◽  
Lamina Propria ◽  
Bowel Disease ◽  
Unknown Etiology ◽  
Tnf Α ◽  
Chronic Enteropathies ◽  
Inflammatory Bowel ◽  
Ifn Γ

Abstract Canine inflammatory bowel disease is a group of chronic enteropathies characterized by persistent or recurring gastric symptoms with an unknown etiology which are related to histopathological changes in the mucosa of the small and large bowel in the form of cellular infiltration in the mucosal lamina propria. Recent years have witnessed a growing number of investigations into the role of the immune system and, in particular, cytokines in the development of IBD. In this article, the expression of pro-inflammatory (IL-1, IL-2, IL-5, IL-6, IL-12, IL-18, IFN-γ, TNF-α) and anti-inflammatory cytokines (IL-4, IL-10) was compared in canine patients with IBD based on clinical presentation, breed, lamina propria cell infiltrate and histopathological grade. Only selected studies confirmed higher mRNA expression levels of cytokines IL-2, IL-4, IL-5, IL-12p40, IFN-γ, TNF-α and TGF-β in dogs with IBD in comparison with healthy subjects. GSD were strongly represented in most study populations. Dogs with LPE were characterized by elevated levels of IL-1α, IL-1β, IL-2, IL-5, IL-6, IL-12, TNF-α, TGF-β. The present studies of canine patients with LPC revealed the mRNA expression of cytokines IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12p35, IL-12p40, IFN-γ, TNF-α, TGF-β. In the reviewed studies, the progression of IBD was not accompanied by changes in the mRNA expression of IL-1α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12, IL-18, TNF-α, IFN-γ or TGF-β.

scholarly journals Tu1734 A Role of iRhom2 for the Secretion of TNF-α in Inflammatory Bowel Disease

2014 ◽  
Vol 146 (5) ◽  
pp. S-829 ◽  
Author(s):  
Sung Wook Hwang ◽  
Jaeyoung Chun ◽  
Changhyun Lee ◽  
Jong Pil Im ◽  
Joo Sung Kim
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Tnf Α ◽  
Inflammatory Bowel

Expression of HLA-DR antigens in inflammatory bowel disease mucosa: Role of intestinal lamina propria mononuclear cell-derived interferon ?

1988 ◽  
Vol 33 (12) ◽  
pp. 1528-1536 ◽  
Author(s):  
Qin Ouyang ◽  
Mounif El-Youssef ◽  
Belinda Yen-Lieberman ◽  
Wanda Sapatnekar ◽  
Kenneth R. Youngman ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Lamina Propria ◽  
Mononuclear Cell ◽  
Bowel Disease ◽  
Intestinal Lamina Propria ◽  
Hla Dr ◽  
Inflammatory Bowel ◽  
Lamina Propria Mononuclear Cell

scholarly journals Psychological Issues in Inflammatory Bowel Disease: An Overview

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
M. S. Sajadinejad ◽  
K. Asgari ◽  
H. Molavi ◽  
M. Kalantari ◽  
P. Adibi
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Illness Behavior ◽  
Unknown Etiology ◽  
Treatment Protocols ◽  
Related Quality ◽  
Health Related ◽  
Inflammatory Bowel ◽  
The Impact

Inflammatory bowel disease (IBD) including Crohn’s disease (CD) and ulcerative colitis (UC) is a chronic and disabling disease with unknown etiology. There have been some controversies regarding the role of psychological factors in the course of IBD. The purpose of this paper is to review that role. First the evidence on role of stress is reviewed focusing on perceived stress and patients’ beliefs about it in triggering or exacerbating the course of IBD. The possible mechanisms by which stress could be translated into IBD symptoms, including changes in motor, sensory and secretory gastrointestinal function, increase intestinal permeability, and changes in the immune system are, then reviewed. The role of patients’ concerns about psychological distress and their adjustment to disease, poor coping strategies, and some personality traits that are commonly associated with these diseases are introduced. The prevalence rate, the timing of onset, and the impact of anxiety and depression on health-related quality of life are then reviewed. Finally issues about illness behavior and the necessity of integrating psychological interventions with conventional treatment protocols are explained.

scholarly journals Immunomodulatory role of Parkinson’s disease 7 in inflammatory bowel disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Rita Lippai ◽  
Apor Veres-Székely ◽  
Erna Sziksz ◽  
Yoichiro Iwakura ◽  
Domonkos Pap ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Inflammatory Bowel Disease ◽  
Parkinson's Disease ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Tnf Α ◽  
Inflammatory Bowel ◽  
Ht 29

AbstractRecently the role of Parkinson’s disease 7 (PARK7) was studied in gastrointestinal diseases, however, the complex role of PARK7 in the intestinal inflammation is still not completely clear. Expression and localization of PARK7 were determined in the colon biopsies of children with inflammatory bowel disease (IBD), in the colon of dextran sodium sulphate (DSS) treated mice and in HT-29 colonic epithelial cells treated with interleukin (IL)-17, hydrogen peroxide (H2O2), tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β or lipopolysaccharide (LPS). Effect of PARK7 on the synthesis of IBD related cytokines was determined using PARK7 gene silenced HT-29 cells and 3,4,5-trimethoxy-N-(4-(8-methylimidazo(1,2-a)pyridine-2-yl)phenyl)benzamide (Comp23)—compound increasing PARK7 activity—treated mice with DSS-colitis. PARK7 expression was higher in the mucosa of children with Crohn’s disease compared to that of controls. While H2O2 and IL-17 treatment increased, LPS, TNF-α or TGF-β treatment decreased the PARK7 synthesis of HT-29 cells. PARK7 gene silencing influenced the synthesis of IL1B, IL6, TNFA and TGFB1 in vitro. Comp23 treatment attenuated the ex vivo permeability of colonic sacs, the clinical symptoms, and mucosal expression of Tgfb1, Il1b, Il6 and Il10 of DSS-treated mice. Our study revealed the role of PARK7 in the regulation of IBD-related inflammation in vitro and in vivo, suggesting its importance as a future therapeutic target.

Role of leptin and TNF-α in energy metabolism regulation in patients with inflammatory bowel disease

2000 ◽  
Vol 32 ◽  
pp. A39
Author(s):  
E. Capristo ◽  
G. Addolorato ◽  
A. Scarfone ◽  
G. Valentini ◽  
G. Mingrone ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Energy Metabolism ◽  
Bowel Disease ◽  
Metabolism Regulation ◽  
Tnf Α ◽  
Inflammatory Bowel

scholarly journals Tenascin-C Is Increased in Inflammatory Bowel Disease and Is Associated with response to Infliximab Therapy

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Longui Ning ◽  
Sha Li ◽  
Jianguo Gao ◽  
Liang Ding ◽  
Chenhui Wang ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Crohn’S Disease ◽  
Disease Activity ◽  
Mrna Expression ◽  
Intestinal Mucosa ◽  
Bowel Disease ◽  
Infliximab Therapy ◽  
Tenascin C ◽  
Inflammatory Bowel

Tenascin-C (TNC) is an extracellular matrix glycoprotein expressed in response to inflammation and tissue damage. The role of TNC in patients with inflammatory bowel disease (IBD) is not well understood. In this study, we analyzed the expression of TNC in the inflamed mucosa of patients with ulcerative colitis (UC) and Crohn’s disease (CD). Serum TNC levels were determined by the enzyme-linked immunosorbent assay (ELISA), and the levels of TNC in patients with different disease activities were compared. The expression of TNC was derived from a GEO dataset. THP-1 cells were stimulated with TNC to evaluate the proinflammatory role of TNC. We found higher TNC expression in the inflamed mucosa of patients with UC and CD compared with normal controls (NCs). TNC was mainly expressed in the stromal area of the intestinal mucosa. The median serum levels of TNC were significantly higher in UC (median 74.1 ng/ml, range 42.6–102.1 ng/ml) and CD (median 59.2 ng/ml, range 44.0–80.9 ng/ml). We also found that serum TNC levels were correlated with Mayo scores in UC and Crohn’s disease activity index (CDAI) in CD. Through GSE14580, we demonstrated that patients who were nonresponsive to infliximab treatment had higher mucosal TNC mRNA expression. High TNC mRNA expression in the inflamed intestinal mucosa was associated with poor response to infliximab therapy in patients with UC. Furthermore, THP-1 cells stimulated with TNC showed increased expression of IL-6, but not TNF-α, IL-8, MCP-1, or IL-1β. Thus, increased TNC levels may participate in the pathogenesis of IBD and may serve as a biomarker for disease activity and response to treatment with infliximab.

scholarly journals Exopolysaccharides from Lactobacillus plantarum YW11 improve immune response and ameliorate inflammatory bowel disease symptoms

2020 ◽  
Author(s):  
Zhang Min ◽  
Hao Xiaona ◽  
Tariq Aziz ◽  
Zhang Jian ◽  
Yang Zhennai
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Body Weight Loss ◽  
Disease Symptoms ◽  
Tnf Α ◽  
Inflammatory Bowel ◽  
Ifn Γ ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine ◽  
Pro Inflammatory Cytokines

Exopolysaccharides (EPSs) possess many bioactivities such as immune regulation, antioxidant, anti-tumor and modulation of intestinal microbial balance but their direct effect on inflammatory bowel disease (IBD) response has not been studied. The purpose of this study was to evaluate the anti-inflammatory effect of EPS produced by L. plantarum YW11 administered at different dosages in IBD mouse model induced with 5% dextran sulphate sodium (DSS). The DSS-induced colitis, accompanied by body weight loss, reduction of colon coefficient and histological colon injury was considerably ameliorated in mice fed the EPS (10 mg/kg). The middle dose of the EPS (25 mg/kg) could effectively recover the intestinal microbial diversity and increase the abundance of Roseburia, Ruminococcus and Blautia with increased content of butyric acid. Moreover, EPS also reduced the production of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IFN-γ, IL-12 and IL-18) and enhanced the anti-inflammatory cytokine IL-10. This study showed that EPS might help in modulation of gut microbiota and improve the immunity of the host to reduce the risk of IBD symptoms.

Molecular evidences on the benefit of N-acetylcysteine in experimental colitis

2008 ◽  
Vol 3 (2) ◽  
pp. 135-142 ◽  
Author(s):  
Fatemeh Ebrahimi ◽  
Hadi Esmaily ◽  
Maryam Baeeri ◽  
Azadeh Mohammadirad ◽  
Saeed Fallah ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Lipid Peroxides ◽  
Experimental Colitis ◽  
Unknown Etiology ◽  
Protective Effects ◽  
Colon Cells ◽  
Antioxidant Power ◽  
Tnf Α ◽  
Inflammatory Bowel

AbstractInflammatory bowel disease (IBD) is a chronic recurrent disease of the digestive tract with an unknown etiology. The aim of this study was to examine the possible protective effects of N-acetylcysteine (NAC) in the mouse model of IBD by measuring specific biomarkers in the colon cells. Colitis was induced by administration of dextran sodium sulfate (DSS) in drinking water (3%) for 7 days. Three doses of NAC (106, 160, and 240 mg/kg) were given after induction of colitis (4 days post DSS) for 4 days by gavage. Lipid peroxides (LP), total antioxidant power (TAP), total thiol molecules (TTM), tumor necrosis factor-α (TNF-α), nitric oxide (NO), superoxide dismutase (SOD), and catalase (CAT) were measured in the colon homogenate of the treated animals. NAC (160 and 240 mg/kg) significantly decreased LP, TNF-α, NO and increased TTM, SOD, and CAT. The TAP was also increased by NAC (240 mg/kg). It is concluded that moderate to high doses of NAC improves cellular biomarkers of IBD in mice. Further studies should be trialled in humans suffering from two common inflammatory bowel disease called ulcerative colitis and Crohn’s disease.

Sign in / Sign up

Export Citation Format

Share Document