Purified rutin and rutin-rich asparagus attenuates disease severity and tissue damage following dextran sodium sulfate-induced colitis

2016 ◽  
Vol 60 (11) ◽  
pp. 2396-2412 ◽  
Author(s):  
Krista A. Power ◽  
Jenifer T. Lu ◽  
Jennifer M. Monk ◽  
Dion Lepp ◽  
Wenqing Wu ◽  
...  
Keyword(s):  
Disease Severity ◽  
Tissue Damage ◽  
Sodium Sulfate ◽  
Dextran Sodium Sulfate

scholarly journals Intrarectal Xyloglucan Administration Reduces Disease Severity in the Dextran Sodium Sulfate Model of Mouse Colitis

2021 ◽  
Vol Volume 14 ◽  
pp. 429-439
Author(s):  
Edward A Ross ◽  
Madelyn H Miller ◽  
Allison Pacheco ◽  
Alicia R Willenberg ◽  
Justine T Tigno-Aranjuez ◽  
...  
Keyword(s):  
Disease Severity ◽  
Sodium Sulfate ◽  
Dextran Sodium Sulfate

Naringin protects against dextran sodium sulfate-induced colitis in mice

Planta Medica ◽  
2010 ◽  
Vol 76 (12) ◽  
Author(s):  
E Giner ◽  
M Marin ◽  
C Recio ◽  
J Ríos ◽  
R Giner
Keyword(s):  
Sodium Sulfate ◽  
Dextran Sodium Sulfate

Comparative effects of STW 5 and STW 5-II in dextran sodium sulfate-induced colitis

Planta Medica ◽  
2013 ◽  
Vol 79 (13) ◽  
Author(s):  
MT Khayyal ◽  
W Wadie ◽  
D Weiser ◽  
H Abdel-Aziz
Keyword(s):  
Sodium Sulfate ◽  
Dextran Sodium Sulfate

scholarly journals Inflammasome Activation Contributes to Interleukin-23 Production in Response to Clostridium difficile

mBio ◽  
2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Carrie A. Cowardin ◽  
Sarah A. Kuehne ◽  
Erica L. Buonomo ◽  
Chelsea S. Marie ◽  
Nigel P. Minton ◽  
...  
Keyword(s):  
Clostridium Difficile ◽  
Disease Severity ◽  
Tissue Damage ◽  
The United States ◽  
Host Cells ◽  
Inflammasome Activation ◽  
Content Type ◽  
Danger Signals ◽  
Interleukin 23 ◽  
Molecular Patterns

ABSTRACT  Clostridium difficileis the most common hospital-acquired pathogen, causing antibiotic-associated diarrhea in over 250,000 patients annually in the United States. Disease is primarily mediated by toxins A and B, which induce potent proinflammatory signaling in host cells and can activate an ASC-containing inflammasome. Recent findings suggest that the intensity of the host response to infection correlates with disease severity. Our lab has identified the proinflammatory cytokine interleukin-23 (IL-23) as a pathogenic mediator during C. difficile infection (CDI). The mechanisms by which C. difficile induces IL-23, however, are not well understood, and the role of toxins A and B in this process is unclear. Here, we show that toxins A and B alone are not sufficient for IL-23 production but synergistically increase the amount of IL-23 produced in response to MyD88-dependent danger signals, including pathogen-associated molecular patterns (PAMPs) and host-derived damage associated molecular patterns (DAMPs). Danger signals also enhanced the secretion of IL-1β in response to toxins A and B, and subsequent IL-1 receptor signaling accounted for the majority of the increase in IL-23 that occurred in the presence of the toxins. Inhibition of inflammasome activation in the presence of extracellular K+likewise decreased IL-23 production. Finally, we found that IL-1β was increased in the serum of patients with CDI, suggesting that this systemic response could influence downstream production of pathogenic IL-23. Identification of the synergy of danger signals with toxins A and B via inflammasome signaling represents a novel finding in the mechanistic understanding of C. difficile-induced inflammation.IMPORTANCEClostridium difficileis among the leading causes of death due to health care-associated infection, and factors determining disease severity are not well understood. C. difficile secretes toxins A and B, which cause inflammation and tissue damage, and recent findings suggest that some of this tissue damage may be due to an inappropriate host immune response. We have found that toxins A and B, in combination with both bacterium- and host-derived danger signals, can induce expression of the proinflammatory cytokines IL-1β and IL-23. Our results demonstrate that IL-1β signaling enhances IL-23 production and could lead to increased pathogenic inflammation during CDI.

scholarly journals Ethanol Extract ofCordyceps militarisGrown on Germinated Soybeans Attenuates Dextran-Sodium-Sulfate- (DSS-) Induced Colitis by Suppressing the Expression of Matrix Metalloproteinases and Inflammatory Mediators

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Dong Ki Park ◽  
Hye-Jin Park
Keyword(s):  
Matrix Metalloproteinases ◽  
Inflammatory Mediators ◽  
Sodium Sulfate ◽  
Activity Index ◽  
Disease Activity Index ◽  
Ethanol Extract ◽  
Treated Group ◽  
Dextran Sodium Sulfate ◽  
Protective Agent ◽  
Colon Tissue

The effect ofCordyceps militaris(CM) grown on germinated soybeans (GSC) in the inflammatory bowel disease (IBD) model was studied. To demonstrate the preventive effect of GSC extract in a dextran-sodium-sulfate- (DSS-) induced acute colitis mouse model, GSC was administered 2 days before DSS coadministration. GSC significantly suppressed DSS-induced disease activity index (DAI) as well as histopathological scores, compared to control or CM-treated group. To elucidate the anti-IBD activity of GSC, we checked the level of matrix metalloproteinases (MMPs) and inflammatory mediators. GSC extract decreased the level of MMP-3 and -9 mRNAs and p53 proteins. The level and activity of LPS-induced MMP-9 were reduced in GSC-treated RAW264.7 cells. It also attenuated the level of inducible nitric oxide synthase (iNOS) and tumor necrosis factor- (TNF-)αmRNAs both in colon tissue and in macrophage cells. These results suggest that GSC can be applied as a protective agent against IBDs.

Sign in / Sign up

Export Citation Format

Share Document