Mouse Models of Acute and Chronic Colitis

Epidermal Growth Factor Partially Restores Colonic Ion Transport Responses in Mouse Models of Chronic Colitis

Gastroenterology ◽

10.1016/j.gastro.2005.06.004 ◽

2005 ◽

Vol 129 (2) ◽

pp. 591-608 ◽

Cited By ~ 48

Author(s):

D MCCOLE ◽

G ROGLER ◽

N VARKI ◽

K BARRETT

Keyword(s):

Growth Factor ◽

Epidermal Growth Factor ◽

Ion Transport ◽

Mouse Models ◽

Chronic Colitis ◽

Epidermal Growth

Download Full-text

Intestinal alkaline phosphatase has beneficial effects in mouse models of chronic colitis

Inflammatory Bowel Diseases ◽

10.1002/ibd.21377 ◽

2011 ◽

Vol 17 (2) ◽

pp. 532-542 ◽

Cited By ~ 54

Author(s):

Sundaram Ramasamy ◽

Deanna D. Nguyen ◽

Michelle A. Eston ◽

Sayeda Nasrin Alam ◽

Angela K. Moss ◽

...

Keyword(s):

Alkaline Phosphatase ◽

Mouse Models ◽

Chronic Colitis ◽

Intestinal Alkaline Phosphatase ◽

Beneficial Effects

Download Full-text

Differential Expression of Soluble Receptor for Advanced Glycation End-products in Mice Susceptible or Resistant to Chronic Colitis

Inflammatory Bowel Diseases ◽

10.1093/ibd/izz311 ◽

2019 ◽

Vol 26 (3) ◽

pp. 360-368 ◽

Cited By ~ 1

Author(s):

Michael Bramhall ◽

Kevin Rich ◽

Ajanta Chakraborty ◽

Larisa Logunova ◽

Namshik Han ◽

...

Keyword(s):

Chronic Inflammation ◽

Mouse Models ◽

Advanced Glycation End Products ◽

Healthy Controls ◽

Advanced Glycation ◽

Chronic Colitis ◽

Trichuris Muris ◽

Soluble Rage ◽

Glycation End Products ◽

End Products

Abstract Background Identifying the factors that contribute to chronicity in inflamed colitic tissue is not trivial. However, in mouse models of colitis, we can investigate at preclinical timepoints. We sought to validate murine Trichuris muris infection as a model for identification of factors that promote development of chronic colitis. Methods We compared preclinical changes in mice with a resolving immune response to T. muris (resistant) vs mice that fail to expel the worms and develop chronic colitis (susceptible). Findings were then validated in healthy controls and patients with suspected or confirmed IBD. Results The receptor for advanced glycation end products (RAGE) was highly dysregulated between resistant and susceptible mice before the onset of any pathological signs. Increased soluble RAGE (sRAGE) in the serum and feces of resistant mice correlated with reduced colitis scores. Mouse model findings were validated in a preliminary clinical study: fecal sRAGE was differentially expressed in patients with active IBD compared with IBD in remission, patients with IBD excluded, or healthy controls. Conclusions Preclinical changes in mouse models can identify early pathways in the development of chronic inflammation that human studies cannot. We identified the decoy receptor sRAGE as a potential mechanism for protection against chronic inflammation in colitis in mice and humans. We propose that the RAGE pathway is clinically relevant in the onset of chronic colitis and that further study of sRAGE in IBD may provide a novel diagnostic and therapeutic target.

Download Full-text

Epidermal Growth Factor Partially Restores Colonic Ion Transport Responses in Mouse Models of Chronic Colitis

Gastroenterology ◽

10.1053/j.gastro.2005.06.004 ◽

2005 ◽

Vol 129 (2) ◽

pp. 591-608

Author(s):

Declan F. McCole ◽

Gerhard Rogler ◽

Nissi Varki ◽

Kim E. Barrett

Keyword(s):

Growth Factor ◽

Epidermal Growth Factor ◽

Ion Transport ◽

Mouse Models ◽

Chronic Colitis ◽

Epidermal Growth

Download Full-text

Differential expression of soluble receptor for advanced glycation end-products (sRAGE) in mice susceptible or resistant to chronic colitis

10.1101/719310 ◽

2019 ◽

Author(s):

Michael Bramhall ◽

Kevin Rich ◽

Ajanta Chakraborty ◽

Larisa Logunova ◽

Namshik Han ◽

...

Keyword(s):

Chronic Inflammation ◽

Mouse Models ◽

Advanced Glycation End Products ◽

Healthy Controls ◽

Advanced Glycation ◽

Chronic Colitis ◽

Trichuris Muris ◽

Soluble Rage ◽

Glycation End Products ◽

End Products

AbstractAimsIdentifying the factors that contribute to chronicity in inflamed colitic tissue is not trivial. However, in mouse models of colitis, we can investigate at preclinical timepoints. We sought to validate murine Trichuris muris infection as a model for identification of factors that promote development of chronic colitis.MethodsWe compared preclinical changes in mice with a resolving immune response to T. muris (resistant) versus mice that fail to expel the worms and develop chronic colitis (susceptible). Findings were then validated in healthy controls and patients with suspected or confirmed IBD.ResultsThe Receptor for Advanced Glycation End Products (Rage) was highly dysregulated between resistant and susceptible mice prior to the onset of any pathological signs. Increased soluble RAGE (sRAGE) in the serum and faeces of resistant mice correlated with reduced colitis scores. Mouse model findings were validated in a preliminary clinical study: faecal sRAGE was differentially expressed in patients with active IBD compared with IBD in remission, patients with IBD excluded or healthy controls.ConclusionPre-clinical changes in mouse models can identify early pathways in the development of chronic inflammation that human studies cannot. We identified the decoy receptor sRAGE as a potential mechanism for protection against chronic inflammation in colitis in mice and humans. We propose that the RAGE pathway is clinically relevant in the onset of chronic colitis, and that further study of sRAGE in IBD may provide a novel diagnostic and therapeutic target.

Download Full-text