scholarly journals Neuroimmunomodulation in the Gut: Focus on Inflammatory Bowel Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Claudio Bernardazzi ◽  
Beatriz Pêgo ◽  
Heitor Siffert P. de Souza
Keyword(s):  
Inflammatory Bowel Disease ◽  
Nervous System ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Critical Role ◽  
Intestinal Immunity ◽  
Intestinal Homeostasis ◽  
Inflammatory Bowel ◽  
Genetic And Environmental Factors ◽  
External Stimuli

Intestinal immunity is finely regulated by several concomitant and overlapping mechanisms, in order to efficiently sense external stimuli and mount an adequate response of either tolerance or defense. In this context, a complex interplay between immune and nonimmune cells is responsible for the maintenance of normal homeostasis. However, in certain conditions, the disruption of such an intricate network may result in intestinal inflammation, including inflammatory bowel disease (IBD). IBD is believed to result from a combination of genetic and environmental factors acting in concert with an inappropriate immune response, which in turn interacts with nonimmune cells, including nervous system components. Currently, evidence shows that the interaction between the immune and the nervous system is bidirectional and plays a critical role in the regulation of intestinal inflammation. Recently, the maintenance of intestinal homeostasis has been shown to be under the reciprocal control of the microbiota by immune mechanisms, whereas intestinal microorganisms can modulate mucosal immunity. Therefore, in addition to presenting the mechanisms underlying the interaction between immune and nervous systems in the gut, here we discuss the role of the microbiota also in the regulation of neuroimmune crosstalk involved in intestinal homeostasis and inflammation, with potential implications to IBD pathogenesis.

scholarly journals Thymus leukemia antigen controls intraepithelial lymphocyte function and inflammatory bowel disease

2008 ◽  
Vol 105 (46) ◽  
pp. 17931-17936 ◽  
Author(s):  
Danyvid Olivares-Villagómez ◽  
Yanice V. Mendez-Fernandez ◽  
Vrajesh V. Parekh ◽  
Saif Lalani ◽  
Tiffaney L. Vincent ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Genetic Model ◽  
Critical Role ◽  
Intraepithelial Lymphocytes ◽  
Lymphocyte Function ◽  
Intestinal Epithelial ◽  
Inflammatory Bowel

Intestinal intraepithelial lymphocytes (IEL) bear a partially activated phenotype that permits them to rapidly respond to antigenic insults. However, this phenotype also implies that IEL must be highly controlled to prevent misdirected immune reactions. It has been suggested that IEL are regulated through the interaction of the CD8αα homodimer with the thymus leukemia (TL) antigen expressed by intestinal epithelial cells. We have generated and characterized mice genetically-deficient in TL expression. Our findings show that TL expression has a critical role in maintaining IEL effector functions. Also, TL deficiency accelerated colitis in a genetic model of inflammatory bowel disease. These findings reveal an important regulatory role of TL in controlling IEL function and intestinal inflammation.

scholarly journals Roles of Autophagy-Related Genes in the Pathogenesis of Inflammatory Bowel Disease

Cells ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 77 ◽  
Author(s):  
Sup Kim ◽  
Hyuk Eun ◽  
Eun-Kyeong Jo
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Paneth Cell ◽  
Conditional Knockout ◽  
Intestinal Homeostasis ◽  
Genetic Studies ◽  
Inflammatory Bowel ◽  
Direct Targeting ◽  
Catabolic Process

Autophagy is an intracellular catabolic process that is essential for a variety of cellular responses. Due to its role in the maintenance of biological homeostasis in conditions of stress, dysregulation or disruption of autophagy may be linked to human diseases such as inflammatory bowel disease (IBD). IBD is a complicated inflammatory colitis disorder; Crohn’s disease and ulcerative colitis are the principal types. Genetic studies have shown the clinical relevance of several autophagy-related genes (ATGs) in the pathogenesis of IBD. Additionally, recent studies using conditional knockout mice have led to a comprehensive understanding of ATGs that affect intestinal inflammation, Paneth cell abnormality and enteric pathogenic infection during colitis. In this review, we discuss the various ATGs involved in macroautophagy and selective autophagy, including ATG16L1, IRGM, LRRK2, ATG7, p62, optineurin and TFEB in the maintenance of intestinal homeostasis. Although advances have been made regarding the involvement of ATGs in maintaining intestinal homeostasis, determining the precise contribution of autophagy has remained elusive. Recent efforts based on direct targeting of ATGs and autophagy will further facilitate the development of new therapeutic opportunities for IBD.

scholarly journals Innate Lymphoid Cells in Intestinal Homeostasis and Inflammatory Bowel Disease

2021 ◽  
Vol 22 (14) ◽  
pp. 7618
Author(s):  
Angela Saez ◽  
Raquel Gomez-Bris ◽  
Beatriz Herrero-Fernandez ◽  
Claudia Mingorance ◽  
Cristina Rius ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cells ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Intestinal Homeostasis ◽  
Mucosal Homeostasis ◽  
Inflammatory Bowel ◽  
Chronic Intestinal Inflammation

Inflammatory bowel disease (IBD) is a heterogeneous state of chronic intestinal inflammation of unknown cause encompassing Crohn’s disease (CD) and ulcerative colitis (UC). IBD has been linked to genetic and environmental factors, microbiota dysbiosis, exacerbated innate and adaptive immunity and epithelial intestinal barrier dysfunction. IBD is classically associated with gut accumulation of proinflammatory Th1 and Th17 cells accompanied by insufficient Treg numbers and Tr1 immune suppression. Inflammatory T cells guide innate cells to perpetuate a constant hypersensitivity to microbial antigens, tissue injury and chronic intestinal inflammation. Recent studies of intestinal mucosal homeostasis and IBD suggest involvement of innate lymphoid cells (ILCs). These lymphoid-origin cells are innate counterparts of T cells but lack the antigen receptors expressed on B and T cells. ILCs play important roles in the first line of antimicrobial defense and contribute to organ development, tissue protection and regeneration, and mucosal homeostasis by maintaining the balance between antipathogen immunity and commensal tolerance. Intestinal homeostasis requires strict regulation of the quantity and activity of local ILC subpopulations. Recent studies demonstrated that changes to ILCs during IBD contribute to disease development. A better understanding of ILC behavior in gastrointestinal homeostasis and inflammation will provide valuable insights into new approaches to IBD treatment. This review summarizes recent research into ILCs in intestinal homeostasis and the latest advances in the understanding of the role of ILCs in IBD, with particular emphasis on the interaction between microbiota and ILC populations and functions.

scholarly journals Neuroinflammation as an etiological trigger for depression comorbid with inflammatory bowel disease

2022 ◽  
Vol 19 (1) ◽  
Author(s):  
Colin F. Craig ◽  
Rhiannon T. Filippone ◽  
Rhian Stavely ◽  
Joel C. Bornstein ◽  
Vasso Apostolopoulos ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Central Nervous System ◽  
Nervous System ◽  
Bowel Disease ◽  
Structural Changes ◽  
Intestinal Inflammation ◽  
In Vivo Models ◽  
The Central Nervous System ◽  
Inflammatory Bowel

AbstractPatients with inflammatory bowel disease (IBD) suffer from depression at higher rates than the general population. An etiological trigger of depressive symptoms is theorised to be inflammation within the central nervous system. It is believed that heightened intestinal inflammation and dysfunction of the enteric nervous system (ENS) contribute to impaired intestinal permeability, which facilitates the translocation of intestinal enterotoxins into the blood circulation. Consequently, these may compromise the immunological and physiological functioning of distant non-intestinal tissues such as the brain. In vivo models of colitis provide evidence of increased blood–brain barrier permeability and enhanced central nervous system (CNS) immune activity triggered by intestinal enterotoxins and blood-borne inflammatory mediators. Understanding the immunological, physiological, and structural changes associated with IBD and neuroinflammation may aid in the development of more tailored and suitable pharmaceutical treatment for IBD-associated depression.

scholarly journals Co-pathogens in Periodontitis and Inflammatory Bowel Disease

2021 ◽  
Vol 8 ◽  
Author(s):  
Zhengwen Cai ◽  
Tao Zhu ◽  
Fengshuo Liu ◽  
Zixuan Zhuang ◽  
Lei Zhao
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Clinical Manifestations ◽  
Fusobacterium Nucleatum ◽  
The Body ◽  
Modes Of Transmission ◽  
Daily Diet ◽  
Inflammatory Bowel ◽  
External Stimuli

Localized inflammatory lesions in one area of the body may affect other distant organs through various modes of transmission thus initiating secondary inflammatory infections. Periodontal disease (PD) and inflammatory bowel disease (IBD) have been shown to coexist. Periodontitis is a multifactorial inflammatory disease, and dental plaque is considered to be the initial risk factor. Individuals with genetic susceptibility are more likely to develop periodontitis when exposed to external stimuli. IBD is affected by host genetics, immunoregulation, daily diet, and the gut microbiota, and its risk factors appear to be shared with those of PD. However, the key etiologies of both diseases remain unclear, thus hindering the exploration of possible links between IBD and PD. Recent studies and systematic reviews have focused on evidence-based statistics of the prevalence and clinical manifestations of both diseases, but discussions of the microbial etiological correlation between periodontitis and intestinal inflammation are scarce. Here, we summarize the potential common pathogenic microorganisms that may serve as bridges between the two diseases. Studies have shown that invasive microorganisms such as Porphyromonas gingivalis, Fusobacterium nucleatum, Klebsiella spp. and Campylobacter spp. play key roles in the comorbidity of PD and IBD.

scholarly journals Resveratrol and inflammatory bowel disease: the evidence so far

2017 ◽  
Vol 31 (1) ◽  
pp. 85-97 ◽  
Author(s):  
Sandra Nunes ◽  
Francesca Danesi ◽  
Daniele Del Rio ◽  
Paula Silva
Keyword(s):  
Inflammatory Bowel Disease ◽  
Intestinal Mucosa ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Human Subjects ◽  
Intestinal Immunity ◽  
Inflammatory Bowel ◽  
Anti Inflammatory

AbstractDespite the fact that inflammatory bowel disease (IBD) has still no recognised therapy, treatments which have proven at least mildly successful in improving IBD symptoms include anti-inflammatory drugs and monoclonal antibodies targeting pro-inflammatory cytokines. Resveratrol, a natural (poly)phenol found in grapes, red wine, grape juice and several species of berries, has been shown to prevent and ameliorate intestinal inflammation. Here, we discuss the role of resveratrol in the improvement of inflammatory disorders involving the intestinal mucosa. The present review covers three specific aspects of resveratrol in the framework of inflammation: (i) its content in food; (ii) its intestinal absorption and metabolism; and (iii) its anti-inflammatory effects in the intestinal mucosa in vitro and in the very few in vivo studies present to date. Actually, if several studies have shown that resveratrol may down-regulate mediators of intestinal immunity in rodent models, only two groups have performed intervention studies in human subjects using resveratrol as an agent to improve IBD conditions. The effects of resveratrol should be further investigated by conducting well-designed clinical trials, also taking into account different formulations for the delivery of the bioactive compound.

scholarly journals Beneficial Role of Fruits, Their Juices, and Freeze-Dried Powders on Inflammatory Bowel Disease and Related Dysbiosis

Plants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 4
Author(s):  
Maria Rosaria Perri ◽  
Carmen Romano ◽  
Mariangela Marrelli ◽  
Ludovica Zicarelli ◽  
Claudia-Crina Toma ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Inflammatory Conditions ◽  
Freeze Dried ◽  
Inflammatory Bowel ◽  
Genetic And Environmental Factors ◽  
In Vivo Effects

Inflammatory bowel disease (IBD) is a group of complex chronic inflammatory conditions affecting the gastrointestinal tract. It is linked to a number of genetic and environmental factors able to perturb the immune-microbiome axis. Diet is the most investigated variable both for its role in the etiology of IBD and for its beneficial potential in the treatment of the symptoms. Dietary products may influence intestinal inflammation through different mechanisms of action, such as the modulation of inflammatory mediators, the alteration of gene expression, changes in gut permeability, and modifications in enteric flora composition. A consisting number of studies deal with the link between nutrition and microbial community, and particular attention is paid to plant-based foods. The effects of the dietary intake of different fruits have been investigated so far. This review aims to present the most recent studies concerning the beneficial potential of fruit consumption on human gut microbiota. Investigated plant species are described, and obtained results are presented and discussed in order to provide an overview of both in vitro and in vivo effects of fruits, their juices, and freeze-dried powders.

scholarly journals Diet–Microbiota Interactions in Inflammatory Bowel Disease

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1533
Author(s):  
Kohei Sugihara ◽  
Nobuhiko Kamada
Keyword(s):  
Inflammatory Bowel Disease ◽  
Gut Microbiota ◽  
Bowel Disease ◽  
Intestinal Inflammation ◽  
Current Knowledge ◽  
Chronic Inflammatory Disease ◽  
Host Cells ◽  
Intestinal Homeostasis ◽  
New Therapeutic Approaches ◽  
Inflammatory Bowel

Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the gastrointestinal tract. Although the precise etiology of IBD is largely unknown, it is widely thought that diet contributes to the development of IBD. Diet shapes the composition of the gut microbiota, which plays critical roles in intestinal homeostasis. In contrast, intestinal inflammation induces gut dysbiosis and may affect the use of dietary nutrients by host cells and the gut microbiota. The interaction of diet and the gut microbiota is perturbed in patients with IBD. Herein, we review the current knowledge of diet and gut microbiota interaction in intestinal homeostasis. We also discuss alterations of diet and gut microbiota interaction that influence the outcome and the nutritional treatment of IBD. Understanding the complex relationships between diet and the gut microbiota provides crucial insight into the pathogenesis of IBD and advances the development of new therapeutic approaches.

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