scholarly journals Role of Mast Cells in Inflammatory Bowel Disease and Inflammation-Associated Colorectal Neoplasia in IL-10-Deficient Mice

PLoS ONE ◽  
2010 ◽  
Vol 5 (8) ◽  
pp. e12220 ◽  
Author(s):  
Maciej Chichlowski ◽  
Greg S. Westwood ◽  
Soman N. Abraham ◽  
Laura P. Hale
2012 ◽  
Vol 302 (11) ◽  
pp. G1322-G1335 ◽  
Author(s):  
Ranyia Matta ◽  
John A. Barnard ◽  
Lyn M. Wancket ◽  
Jing Yan ◽  
Jianjing Xue ◽  
...  

Il-10-deficient mice develop colitis associated with exaggerated Th1/Th17 responses and are a valuable model of inflammatory bowel disease. Mkp-1 is a major negative regulator of MAPKs, and its expression is enhanced by IL-10. To understand the role of Mkp-1 in the regulation of intestinal mucosal immune responses, we studied the effect of Mkp-1 deletion on the pathogenesis of colitis in Il-10−/−mice. We found that knockout of Mkp-1 on an Il-10−/−background accelerated the development of colitis. Compared with Il-10−/−mice, colitis not only appeared earlier but also was more severe in Il-10−/−/ Mkp-1−/−mice. Il-10−/−mice exhibited a mild intestinal inflammation in the specific pathogen-free environment, and rectal prolapse rarely appeared before 6 mo of age. In contrast, the majority of Il-10−/−/ Mkp-1−/−mice developed severe colitis rapidly and presented with rectal prolapse after only 2–3 mo. The colon of Il-10−/−/ Mkp-1−/−mice showed diffuse transmural chronic inflammation and mucosal hyperplasia, with significantly more proliferating crypt epithelial cells than those of Il-10−/−mice. In addition to the severe colitis, Il-10−/−/ Mkp-1−/−mice also developed conjunctivitis and blepharitis. The colon of Il-10−/−/ Mkp-1−/−mice contained significantly higher levels of proinflammatory cytokines and exhibited greater MAPK activities than did the colon of Il-10−/−mice. Splenocytes and lymphocytes from Il-10−/−/ Mkp-1−/−mice produced higher levels of Th1 cytokines ex vivo upon activation than did cells from Il-10−/−mice. Our studies support a pivotal role of Mkp-1 as a negative regulator of mucosal immune responses and highlight its protective function against inflammatory bowel disease.


2001 ◽  
Vol 120 (5) ◽  
pp. A523-A523
Author(s):  
A BURICH ◽  
R HERSHBERG ◽  
K WAGGIE ◽  
W ZENG ◽  
J VINEY ◽  
...  

2009 ◽  
Vol 47 (09) ◽  
Author(s):  
J Glas ◽  
J Seiderer ◽  
HP Török ◽  
B Göke ◽  
T Ochsenkühn ◽  
...  

2009 ◽  
Vol 150 (18) ◽  
pp. 839-845 ◽  
Author(s):  
János Banai

Aetiology of inflammatory bowel disease (IBD) is complex and probably multifactorial. Nutrition has been proposed to be an important aetiological factor for development of IBD. Several components of the diet (such as sugar, fat, fibre, fruit and vegetable, protein, fast food, preservatives etc.) were examined as possible causative agents for IBD. According to some researchers infant feeding (breast feeding) may also contribute to the development of IBD. Though the importance of environmental factors is evidenced by the increasing incidence in developed countries and in migrant population in recent decades, the aetiology of IBD remained unclear. There are many theories, but as yet no dietary approaches have been proved to reduce the risk of developing IBD. The role of nutrition in the management of IBD is better understood. The prevention and correction of malnutrition, the provision of macro- and micronutrients and vitamins and the promotion of optimal growth and development of children are key points of nutritional therapy. In active disease, the effective support of energy and nutrients is a very important part of the therapy. Natural and artificial nutrition or the combination of two can be choosen for supporting therapy of IBD. The author summarises the aetiological and therapeutic role of nutrition in IBD.


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