scholarly journals Microbiota in mesenteric adipose tissue from Crohn’s disease promote colitis in mice

Microbiome ◽  
2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Zhen He ◽  
Jinjie Wu ◽  
Junli Gong ◽  
Jia Ke ◽  
Tao Ding ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Ribosomal Rna ◽  
Intestinal Inflammation ◽  
Multidimensional Data ◽  
Mesenteric Adipose Tissue ◽  
Pathologic Characteristic ◽  
Metabolites Production ◽  
Colitis Model

Abstract Background Mesenteric adipose tissue (mAT) hyperplasia, known as creeping fat is a pathologic characteristic of Crohn’s disease (CD). The reserve of creeping fat in surgery is associated with poor prognosis of CD patients, but the mechanism remains unknown. Methods Mesenteric microbiome, metabolome, and host transcriptome were characterized using a cohort of 48 patients with CD and 16 non-CD controls. Multidimensional data including 16S ribosomal RNA gene sequencing (16S rRNA), host RNA sequencing, and metabolome were integrated to reveal network interaction. Mesenteric resident bacteria were isolated from mAT and functionally investigated both in the dextran sulfate sodium (DSS) model and in the Il10 gene-deficient (Il10−/−) mouse colitis model to validate their pro-inflammatory roles. Results Mesenteric microbiota contributed to aberrant metabolites production and transcripts in mATs from patients with CD. The presence of mAT resident microbiota was associated with the development of CD. Achromobacter pulmonis (A. pulmonis) isolated from CD mAT could translocate to mAT and exacerbate both DSS-induced and Il10 gene-deficient (Il10−/−) spontaneous colitis in mice. The levels of A. pulmonis in both mAT and mucous layer from CD patients were higher compared to those from the non-CD group. Conclusions This study suggests that the mesenteric microbiota from patients with CD sculpt a detrimental microenvironment and promote intestinal inflammation.

scholarly journals Microbiota in Mesenteric Adipose Tissue From Crohn’s Disease Promote Colitis in Mice

2021 ◽  
Author(s):  
Zhen He ◽  
Jinjie Wu ◽  
Junli Gong ◽  
Jia Ke ◽  
Tao Ding ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Ribosomal Rna ◽  
Intestinal Inflammation ◽  
Multidimensional Data ◽  
Mesenteric Adipose Tissue ◽  
Pathologic Characteristic ◽  
Metabolites Production ◽  
Colitis Model

Abstract Background: Mesenteric adipose tissue (mAT) hyperplasia, known as creeping fat is a pathologic characteristic of Crohn’s disease (CD). The reserve of creeping fat in surgery is associated with poor prognosis of CD patients, but the mechanism remains unknown.Methods: Mesenteric microbiome, metabolome and host transcriptome were characterized using a cohort of 48 patients with CD and 16 non-CD controls. Multidimensional data including 16S ribosomal RNA gene sequencing (16S rRNA), host RNA sequencing and metabolome were integrated to reveal network interaction. Mesenteric resident bacteria were isolated from mAT and functionally investigated both in dextran sulfate sodium (DSS) model and Il10 gene deficient (Il10-/-) mouse colitis model to validate their pro-inflammatory roles. Results: Mesenteric microbiota contributed to aberrant metabolites production and transcripts in mATs from patients with CD. Presence of mAT resident microbiota was associated with the development of CD. Achromobacter pulmonis (A. pulmonis) isolated from CD mAT could translocate to mAT and exacerbate both DSS-induced and Il10 gene deficient (Il10-/-) spontaneous colitis in mice. The levels of A. pulmonis both in mAT and mucous layer from CD patients were higher compared to those from non-CD group. Conclusions: This study suggests that the mesenteric microbiota from patients with CD sculpt a detrimental microenvironment and promote intestinal inflammation.

scholarly journals The Role of Mesenteric Adipose Tissue in Crohn’s Disease

2018 ◽  
Author(s):  
Raquel Franco Leal ◽  
Lívia Bitencourt Pascoal ◽  
Francesca Aparecida Ramos da Silva ◽  
Bruno Lima Rodrigues
Keyword(s):  
Adipose Tissue ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Mesenteric Adipose Tissue

scholarly journals ER stress activation in the intestinal mucosa but not in mesenteric adipose tissue is associated with inflammation in Crohn’s disease patients

PLoS ONE ◽  
2019 ◽  
Vol 14 (9) ◽  
pp. e0223105 ◽  
Author(s):  
Andressa Coope ◽  
Lívia Bitencourt Pascoal ◽  
José Diego Botezelli ◽  
Francesca Aparecida Ramos da Silva ◽  
Maria de Lourdes Setsuko Ayrizono ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Er Stress ◽  
Intestinal Mucosa ◽  
Mesenteric Adipose Tissue ◽  
Stress Activation

scholarly journals Long-term changes in adipose tissue in human disease

2001 ◽  
Vol 60 (3) ◽  
pp. 365-374 ◽  
Author(s):  
Caroline M. Pond
Keyword(s):  
Adipose Tissue ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Lymph Nodes ◽  
Immune Cells ◽  
Lymphoid Cells ◽  
Dietary History ◽  
Mesenteric Adipose Tissue ◽  
Long Term Changes

Redistribution of white adipose tissue is a long-term symptom of several chronic diseases. Although the roles of adipocytes in acute illness have been thoroughly studied, how or why short-term responses of adipose tissue to disease sometimes produce long-term redistribution, and the causal relationship between the anatomical changes and the associated metabolic syndromes are poorly understood. The present paper reviews explanations for the redistribution of adipose tissue after infection with HIV, and in Crohn's disease; both conditions that share the peculiarity of selective expansion of certain adipose depots while others are depleted. HIV adipose tissue redistribution syndrome (HARS) develops gradually after several months of infection with the HIV both in untreated patients and in those taking protease inhibitors and nucleoside reverse transcriptase inhibitors. Some current theories about the causes of HARS are critically assessed, and reasons presented for implicating local interactions between the immune system and perinodal adipocytes. Some evolutionary aspects of conspicuous long-term changes in the distribution of human adipose tissue are discussed. Adipose tissue acts as a social signal, indicating dietary history and previous exposure to pathogens. A distinctive symptom of Crohn's disease is selective enlargement of the mesenteric adipose tissue near the diseased lymph nodes and intestine. Perinodal adipocytes have site-specific properties not found in adipocytes from nodeless depots, such as perirenal and epididymal, that may equip them to interact locally with lymph-node lymphoid cells, making polyunsaturated fatty acids selectively and rapidly available to activated immune cells. Studies of the time course of activation of perinodal adipocytes via the lymph nodes they enclose indicate that prolonged or frequent stimulation recruits more adipocytes to control by immune cells, which may lead to selective enlargement of node-containing depots. These concepts suggest hypotheses about HARS and the anomalous development of mesenteric adipose tissue in Crohn's disease that could form the basis for further investigations.

Evaluation of the Pro-Inflammatory ER Stress Activation in Intestinal Mucosa and Mesenteric Adipose Tissue in Crohn's Disease Patients

2017 ◽  
Vol 152 (5) ◽  
pp. S763
Author(s):  
Andressa Coope ◽  
José Diego Botezelli ◽  
Lívia A. Pascoal ◽  
Francesca R. Silva ◽  
Maria de Lourdes S. Ayrizono ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Er Stress ◽  
Intestinal Mucosa ◽  
Mesenteric Adipose Tissue ◽  
Stress Activation

scholarly journals Role of Obesity, Mesenteric Adipose Tissue, and Adipokines in Inflammatory Bowel Diseases

Biomolecules ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 780 ◽  
Author(s):  
Jan Bilski ◽  
Agnieszka Mazur-Bialy ◽  
Dagmara Wojcik ◽  
Marcin Surmiak ◽  
Marcin Magierowski ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Inflammatory Bowel Diseases ◽  
Special Role ◽  
Mesenteric Adipose Tissue ◽  
Bowel Diseases ◽  
Inflammatory Bowel

Inflammatory bowel diseases (IBDs) are a group of disorders which include ulcerative colitis and Crohn’s disease. Obesity is becoming increasingly more common among patients with inflammatory bowel disease and plays a role in the development and course of the disease. This is especially true in the case of Crohn’s disease. The recent results indicate a special role of visceral adipose tissue and particularly mesenteric adipose tissue, also known as “creeping fat”, in pathomechanism, leading to intestinal inflammation. The involvement of altered adipocyte function and the deregulated production of adipokines, such as leptin and adiponectin, has been suggested in pathogenesis of IBD. In this review, we discuss the epidemiology and pathophysiology of obesity in IBD, the influence of a Western diet on the course of Crohn’s disease and colitis in IBD patients and animal’s models, and the potential role of adipokines in these disorders. Since altered body composition, decrease of skeletal muscle mass, and development of pathologically changed mesenteric white adipose tissue are well-known features of IBD and especially of Crohn’s disease, we discuss the possible crosstalk between adipokines and myokines released from skeletal muscle during exercise with moderate or forced intensity. The emerging role of microbiota and the antioxidative and anti-inflammatory enzymes such as intestinal alkaline phosphatase is also discussed, in order to open new avenues for the therapy against intestinal perturbations associated with IBD.

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