scholarly journals Inflammatory Bowel Disease: A Potential Result from the Collusion between Gut Microbiota and Mucosal Immune System

2019 ◽  
Vol 7 (10) ◽  
pp. 440 ◽  
Author(s):  
Bei Yue ◽  
Xiaoping Luo ◽  
Zhilun Yu ◽  
Sridhar Mani ◽  
Zhengtao Wang ◽  
...  

Host health depends on the intestinal homeostasis between the innate/adaptive immune system and the microbiome. Numerous studies suggest that gut microbiota are constantly monitored by the host mucosal immune system, and any slight disturbance in the microbial communities may contribute to intestinal immune disruption and increased susceptibility to inflammatory bowel disease (IBD), a chronic relapsing inflammatory condition of the gastrointestinal tract. Therefore, maintaining intestinal immune homeostasis between microbiota composition and the mucosal immune system is an effective approach to prevent and control IBD. The overall theme of this review is to summarize the research concerning the pathogenesis of IBD, with particular focus on the factors of gut microbiota-mucosal immune interactions in IBD. This is a comprehensive and in-depth report of the crosstalk between gut microbiota and the mucosal immune system in IBD pathogenesis, which may provide insight into the further evaluation of the therapeutic strategies for IBD.

2017 ◽  
Vol 18 (10) ◽  
pp. 2020 ◽  
Author(s):  
Grainne Holleran ◽  
Loris Lopetuso ◽  
Valentina Petito ◽  
Cristina Graziani ◽  
Gianluca Ianiro ◽  
...  

2011 ◽  
Vol 300 (5) ◽  
pp. G716-G722 ◽  
Author(s):  
Silvio Danese

Inflammatory bowel disease (IBD) pathogenesis is driven by the interactions between the innate and the adaptive immune system. Both systems are actually expressed not only by immune cells, but also by essentially all types of nonimmune cells. Nonimmune cells have classically been considered as simple targets of the aberrant inflammatory process occurring in IBD. However, the discovery that many of the functions traditionally attributed to immune cells are also performed by nonimmune cells has caused a shift to a multidirectional hypothesis in which nonimmune cells and even acellular elements are considered active players of IBD pathogenesis. The aim of this review is to summarize the current role played by each cell type in IBD pathogenesis.


2020 ◽  
Vol 25 (46) ◽  
pp. 4893-4913 ◽  
Author(s):  
Fan Cao ◽  
Jie Liu ◽  
Bing-Xian Sha ◽  
Hai-Feng Pan

: Inflammatory bowel disease (IBD) is a chronic, elusive disorder resulting in relapsing inflammation of intestine with incompletely elucidated etiology, whose two representative forms are ulcerative colitis (UC) and Crohn’s disease (CD). Accumulating researches have revealed that the individual genetic susceptibility, environmental risk elements, intestinal microbial flora, as well as innate and adaptive immune system are implicated in the pathogenesis and development of IBD. Despite remarkable progression of IBD therapy has been achieved by chemical drugs and biological therapies such as aminosalicylates, corticosteroids, antibiotics, anti-tumor necrosis factor (TNF)-α, anti-integrin agents, etc., healing outcome still cannot be obtained, along with inevitable side effects. Consequently, a variety of researches have focused on exploring new therapies, and found that natural products (NPs) isolated from herbs or plants may serve as promising therapeutic agents for IBD through antiinflammatory, anti-oxidant, anti-fibrotic and anti-apoptotic effects, which implicates the modulation on nucleotide- binding domain (NOD) like receptor protein (NLRP) 3 inflammasome, gut microbiota, intestinal microvascular endothelial cells, intestinal epithelia, immune system, etc. In the present review, we will summarize the research development of IBD pathogenesis and current mainstream therapy, as well as the therapeutic potential and intrinsic mechanisms of NPs in IBD.


Physiology ◽  
2001 ◽  
Vol 16 (6) ◽  
pp. 272-277 ◽  
Author(s):  
F. Stephen Laroux ◽  
Kevin P. Pavlick ◽  
Robert E. Wolf ◽  
Matthew B. Grisham

The mucosal interstitia of the intestine and colon are continuously exposed to large amounts of dietary and microbial antigens. Fortunately, the mucosal immune system has evolved efficient mechanisms to distinguish potentially pathogenic from nonpathological antigens. There are, however, situations in which this immune regulation fails, resulting in chronic gut inflammation.


2017 ◽  
Vol 152 (5) ◽  
pp. S111
Author(s):  
Amy Tsou ◽  
Jeremy A. Goettel ◽  
Amlan Biswas ◽  
YuHui Kang ◽  
Jeffrey Saltzman ◽  
...  

2011 ◽  
Vol 33 (4) ◽  
pp. 26-31
Author(s):  
Mona Bajaj-Elliott

Intestinal homoeostasis is a complex affair. We are just beginning to appreciate the molecular nature of the crosstalk that allows happy coexistence between the commensal resident microbiota and the gastrointestinal (GI) mucosal immune system. Both microbial and host components involved in this interplay are being increasingly identified and studied. A better understanding of these multifaceted interactions holds the key for unlocking the cellular events responsible for gut inflammatory conditions such as Crohn's disease and ulcerative colitis.


Author(s):  
Valentina Guarnotta ◽  
Rosario Ferrigno ◽  
Marianna Martino ◽  
Mattia Barbot ◽  
Andrea M. Isidori ◽  
...  

Abstract The pandemic of coronavirus disease (COVID-19), a disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is causing high and rapid morbidity and mortality. Immune system response plays a crucial role in controlling and resolving the viral infection. Exogenous or endogenous glucocorticoid excess is characterized by increased susceptibility to infections, due to impairment of the innate and adaptive immune system. In addition, diabetes, hypertension, obesity and thromboembolism are conditions overrepresented in patients with hypercortisolism. Thus patients with chronic glucocorticoid (GC) excess may be at high risk of developing COVID-19 infection with a severe clinical course. Care and control of all comorbidities should be one of the primary goals in patients with hypercortisolism requiring immediate and aggressive treatment. The European Society of Endocrinology (ESE), has recently commissioned an urgent clinical guidance document on management of Cushing’s syndrome in a COVID-19 period. In this review, we aim to discuss and expand some clinical points related to GC excess that may have an impact on COVID-19 infection, in terms of both contagion risk and clinical outcome. This document is addressed to all specialists who approach patients with endogenous or exogenous GC excess and COVID-19 infection.


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