Treatment with Bifidobacterium longum 51A attenuates intestinal damage and inflammatory response in experimental colitis

2020 ◽  
Vol 11 (1) ◽  
pp. 47-57 ◽  
Author(s):  
F.A. Abrantes ◽  
B.B. Nascimento ◽  
M.E.R. Andrade ◽  
P.A.V. de Barros ◽  
C.T. Cartelle ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Intestinal Permeability ◽  
Bifidobacterium Longum ◽  
Experimental Colitis ◽  
Sodium Sulphate ◽  
Intestinal Damage ◽  
Dextran Sodium Sulphate ◽  
Eosinophil Peroxidase ◽  
Total Treatment ◽  
Disease Induction

This study evaluated the effects of Bifidobacterium longum 51A on the intestinal mucosa and inflammatory response in experimental colitis. Colitis was induced by administration of 3.5% dextran sodium sulphate (DSS) solution for 7 days. Two periods of administration were performed: treatment (T) group, mice received Bifidobacterium only during disease induction (7 days); total treatment (TT) group, mice received Bifidobacterium for 10 days before and during disease induction. The probiotic effects on intestinal permeability, inflammatory infiltrate, histological analysis, cytokines, chemokines and sIgA were evaluated. Bifidobacterium administration in the T group showed reduction in intestinal permeability and lower IL-1β, myeloperoxidase, and eosinophil peroxidase levels compared to those in the colitis group (P<0.05). Bifidobacterium administration in the TT group attenuated severe lesions in the colon and reduced eosinophil peroxidase level (P<0.05). B. longum 51A treatment modality was more effective than total treatment and reduced the inflammatory response and its consequences on intestinal epithelium.

scholarly journals Ablation of ceramide synthase 2 exacerbates dextran sodium sulphate-induced colitis in mice due to increased intestinal permeability

2017 ◽  
Vol 21 (12) ◽  
pp. 3565-3578 ◽  
Author(s):  
Ye-Ryung Kim ◽  
Giora Volpert ◽  
Kyong-Oh Shin ◽  
So-Yeon Kim ◽  
Sun-Hye Shin ◽  
...  
Keyword(s):  
Intestinal Permeability ◽  
Sodium Sulphate ◽  
Ceramide Synthase ◽  
Dextran Sodium Sulphate

scholarly journals Somatostatin does not attenuate intestinal injury in dextran sodium sulphate-induced subacute colitis

1998 ◽  
Vol 7 (3) ◽  
pp. 169-173 ◽  
Author(s):  
J. D. van Bergeijk ◽  
M. E. van Meeteren ◽  
C. J. A. M. Tak ◽  
A. P. M. van Dijk ◽  
M. A. C. Meijssen ◽  
...  
Keyword(s):  
Intestinal Inflammation ◽  
Experimental Colitis ◽  
Sodium Sulphate ◽  
Dextran Sodium Sulphate ◽  
Acute Colitis ◽  
Inflammatory Score ◽  
Long Acting ◽  
Intestinal Macrophage

From severalin vitroandin vivostudies involvement of som atostatin (SMS) in intestinal inflammation emerge. Acute colitis induced in rats is attenuated by the long-acting SMS analogue octreotide. We studied the potential beneficial effect of SMS on non-acute experimental colitis. BALB/c mice received either saline, SMS-14 (36 or 120 μg daily) or octreotide (3 μg daily) subcutaneously delivered by implant osmotic pumps. A non-acute colitis was induced by administration of dextran sodium sulphate (DSS) 10% in drinking water during 7 days. DSS evoked a mild, superficial pancolitis, most characterized by mucosal ulceration and submucosal influx of neutrophils. Neither SMS-14 nor octreotide reduced mucosal inflammatory score or macroscopical disease activity, although reduction of intestinal levels of interleukin1 β (IL-1 β), IL-6 and IL-10 during DSS was augmented both by SMS and octreotide. A slight increase of neutrophil influx was seen during SMS administration in animals not exposed to DSS. In conclusion, SMS or its long-acting analogue did not reduce intestinal inflammation in non-acute DSS-induced colitis. According to the cytokine profile observed, SMS-14 and octreotide further diminished the reduction of intestinal macrophage and Th2 lymphocyte activity.

scholarly journals The role of sodium thiocyanate supplementation during dextran sodium sulphate-stimulated experimental colitis

2020 ◽  
Vol 692 ◽  
pp. 108490 ◽  
Author(s):  
Yuyang Liu ◽  
Thomas Burton ◽  
Benjamin Saul Rayner ◽  
Patrick T. San Gabriel ◽  
Han Shi ◽  
...  
Keyword(s):  
Experimental Colitis ◽  
Sodium Sulphate ◽  
Sodium Thiocyanate ◽  
Dextran Sodium Sulphate

New biomarkers for increased intestinal permeability induced by dextran sodium sulphate and fasting in chickens

2016 ◽  
Vol 101 (5) ◽  
pp. e237-e245 ◽  
Author(s):  
S. Gilani ◽  
G. S. Howarth ◽  
S. M. Kitessa ◽  
C. D. Tran ◽  
R. E. A. Forder ◽  
...  
Keyword(s):  
Intestinal Permeability ◽  
Sodium Sulphate ◽  
Dextran Sodium Sulphate ◽  
New Biomarkers

scholarly journals Antioxidative and immunomodulatory effects of tributyrin supplementation on experimental colitis

2012 ◽  
Vol 109 (8) ◽  
pp. 1396-1407 ◽  
Author(s):  
Alda J. Leonel ◽  
Lílian G. Teixeira ◽  
Rafael P. Oliveira ◽  
Andrezza F. Santiago ◽  
Nathália V. Batista ◽  
...  
Keyword(s):  
Intestinal Permeability ◽  
Transforming Growth Factor ◽  
Control Diet ◽  
Experimental Colitis ◽  
Transforming Growth Factor Β ◽  
Mucosal Damage ◽  
Sodium Sulphate ◽  
Positive Effects ◽  
Anti Inflammatory

Tributyrin (TBT) is a TAG composed of three butyric acids that has beneficial effects on ulcerative colitis due to its trophic, anti-inflammatory, pro-apoptotic and anti-carcinogenic properties. The goal of the present study was to evaluate the efficacy and mechanisms of action of TBT supplementation in the prevention of mucosal damage in experimental colitis. Mice received either a control diet or a TBT-supplemented diet for 15 d. Colitis was induced by dextran sodium sulphate administration during the last 7 d. Mucosal damage and the activation of immune cells and cytokines were determined by histological score, flow cytometry and ELISA. Leucocyte rolling and adhesion were assessed by intravital microscopy. Oxidative stress was determined by monitoring hydroperoxide concentration and evaluating superoxide dismutase (SOD) and catalase activities. Intestinal permeability was analysed using diethylenetriaminepentaacetate acid (99mTcDTPA). Compared with the colitis group, the animals in the colitis+TBT group had reduced mucosal damage and neutrophil and eosinophil mucosal infiltration, which were associated with a higher percentage of regulatory T cells (Treg) and higher levels of transforming growth factor β and IL-10 in the lamina propria. The level ofin vivoleucocyte adhesion in the colon microvasculature was reduced after TBT supplementation. A lower level of hydroperoxide and higher levels of SOD and catalase activities were associated with TBT supplementation. TBT-supplemented mice showed reduced intestinal permeability to the levels intermediate between the control and colitis groups. In conclusion, the present results show that TBT has positive effects on colonic restructuring in experimental colitis. Additionally, TBT supplementation changes the immune response by controlling inflammation and regulating the expression of anti-inflammatory cytokines and Treg.

scholarly journals Titanium Dioxide Presents a Different Profile in Dextran Sodium Sulphate-Induced Experimental Colitis in Mice Lacking the IBD Risk Gene Ptpn2 in Myeloid Cells

2021 ◽  
Vol 22 (2) ◽  
pp. 772
Author(s):  
Javier Conde ◽  
Marlene Schwarzfischer ◽  
Egle Katkeviciute ◽  
Janine Häfliger ◽  
Anna Niechcial ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Titanium Dioxide ◽  
Genetic Risk ◽  
Intestinal Inflammation ◽  
Sodium Sulphate ◽  
Food Additive ◽  
Wild Type ◽  
Dextran Sodium Sulphate ◽  
Risk Gene ◽  
The Impact

Environmental and genetic factors have been demonstrated to contribute to the development of inflammatory bowel disease (IBD). Recent studies suggested that the food additive; titanium dioxide (TiO2) might play a causative role in the disease. Therefore, in the present study we aimed to explore the interaction between the food additive TiO2 and the well-characterized IBD risk gene protein tyrosine phosphatase non-receptor type 2 (Ptpn2) and their role in the development of intestinal inflammation. Dextran sodium sulphate (DSS)-induced acute colitis was performed in mice lacking the expression of Ptpn2 in myeloid cells (Ptpn2LysMCre) or their wild type littermates (Ptpn2fl/fl) and exposed to the microparticle TiO2. The impact of Ptpn2 on TiO2 signalling pathways and TiO2-induced IL-1β and IL-10 levels were studied using bone marrow-derived macrophages (BMDMs). Ptpn2LysMCre exposed to TiO2 exhibited more severe intestinal inflammation than their wild type counterparts. This effect was likely due to the impact of TiO2 on the differentiation of intestinal macrophages, suppressing the number of anti-inflammatory macrophages in Ptpn2 deficient mice. Moreover, we also found that TiO2 was able to induce the secretion of IL-1β via mitogen-activated proteins kinases (MAPKs) and to repress the expression of IL-10 in bone marrow-derived macrophages via MAPK-independent pathways. This is the first evidence of the cooperation between the genetic risk factor Ptpn2 and the environmental factor TiO2 in the regulation of intestinal inflammation. The results presented here suggest that the ingestion of certain industrial compounds should be taken into account, especially in individuals with increased genetic risk

scholarly journals Orally administered RDP58 reduces the severity of dextran sodium sulphate induced colitis

2002 ◽  
Vol 61 (Supplement 2) ◽  
pp. 19ii-24 ◽  
Author(s):  
R Boismenu ◽  
Y Chen ◽  
K Chou ◽  
A El-Sheikh ◽  
R Buelow
Keyword(s):  
Sodium Sulphate ◽  
Dextran Sodium Sulphate
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