Protective and anti-inflammatory role of REG1A in inflammatory bowel disease induced by JAK/STAT3 signaling axis

2021 ◽  
Vol 92 ◽  
pp. 107304
Author(s):  
Hongli Mao ◽  
Jinlin Jia ◽  
Jinxiu Sheng ◽  
Shanfeng Zhang ◽  
Kaida Huang ◽  
...  
2020 ◽  
Vol 21 (16) ◽  
pp. 5801 ◽  
Author(s):  
Dania AlQasrawi ◽  
Ahmad Qasem ◽  
Saleh A. Naser

Cigarette smoke (CS) has adverse effects in patients with Crohn’s disease (CD), an inflammatory bowel disease (IBD) that has been associated with microbial infection, immuno-dysregulation, and mucosal dysfunction. However, CS seems to provide relief and protection to patients with another IBD known as ulcerative colitis (UC). These two subsets are featured as M1- and M2-mediated responses, respectively. Nicotine is the most active, addictive, and studied ingredient in CS. The mechanism of how nicotine and/or other CS ingredients induce pro-inflammatory or anti-inflammatory phenotypes in IBD patients remains under investigation. Our most recent in vitro nicotine study provided significant insights toward understanding the contradictory effects of nicotine on IBD patients, and it elucidated the mechanistic role of α7nAChR in modulation of macrophages in tobacco smokers. Shifting the beneficial effect of nicotine to a harmful outcome in CD patients was linked to a nicotine-microbe interaction that supports a microbial etiology in CD pathogenesis. Among the most debated pathogens in CD etiology is Mycobacterium avium subspecies paratuberculosis (MAP). Other studies associated nicotine with upregulation of miR-124 expression in macrophages, which led to anti-inflammatory response. This review discusses published work on the role of nicotine in modulation of the innate immune response and subsequent signaling in macrophages in IBD subsets.


Author(s):  
Masashi Ohno ◽  
Takayuki Imai ◽  
Motoharu Chatani ◽  
Atsushi Nishida ◽  
Osamu Inatomi ◽  
...  

2018 ◽  
Vol 154 (6) ◽  
pp. S-1017
Author(s):  
Shuko Iwatani ◽  
Shinichiro Shinzaki ◽  
Hideki Iijima ◽  
Yuriko Otake ◽  
Mizuki Tani ◽  
...  

2013 ◽  
Vol 108 ◽  
pp. S526
Author(s):  
Millie Long ◽  
Michael Kappelman ◽  
Christopher Martin ◽  
Wenli Chen ◽  
Kristen Anton ◽  
...  

2016 ◽  
Vol 50 (2) ◽  
pp. 152-156 ◽  
Author(s):  
Millie D. Long ◽  
Michael D. Kappelman ◽  
Christopher F. Martin ◽  
Wenli Chen ◽  
Kristen Anton ◽  
...  

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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