The Mesentery, Systemic Inflammation, and Crohn’s Disease

Rivera, Edgardo D Rivera; Coffey, J. Calvin; Walsh, Dara; Ehrenpreis, Eli D.

doi:10.1093/ibd/izy201

Cited by 74 publications

(56 citation statements)

References 71 publications

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“…Mesenteric findings on CT enterography were reported to be a more critical predictor of endoscopic severity of ulceration in CD than mural findings . Some authors have also reported that combined resection of the mesentery could reduce cumulative reoperation rates compared with standard bowel resection in CD (40% vs 2.9%) . It is still unknown whether abnormalities in the mesentery are primary or secondary phenomena of intestinal inflammation in CD.…”

Section: Discussionmentioning

confidence: 99%

Difference in the frequency of pouchitis between ulcerative colitis and familial adenomatous polyposis: is the explanation in peripouch fat?

Xian

Khan

et al. 2019

Colorectal Disease

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Aim Patients with ulcerative colitis (UC) have an unexplained higher incidence of pouchitis and a greater amount of peripouch fat compared with patients with familial adenomatous polyposis (FAP). The aims of this study were to compare the peripouch fat areas between patients with UC and patients with FAP, and to explore relationship between peripouch fat and pouchitis or chronic antibiotic-refractory pouchitis (CARP). ConclusionOur study demonstrates that patients with UC have more peripouch fat than those with FAP, which may explain the difference in the frequency of pouchitis and CARP between these groups of patients.What does this paper add to the literature? Pouchitis occurs frequently in patients with ulcerative colitis, but seldom in patients with familial adenomatous polyposis. We describe a new method for measuring peripouch fat using CT images and found that peripouch fat was likely to be the determining factor in pouchitis. It suggests that we can use peripouch fat to predict pouchitis.

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Section: Discussionmentioning

confidence: 99%

Difference in the frequency of pouchitis between ulcerative colitis and familial adenomatous polyposis: is the explanation in peripouch fat?

Xian

Khan

et al. 2019

Colorectal Disease

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“…10000x magnification; (C) Fragment of adipocyte, with large fat droplet in adipocyte (4) and hemocapillary (7). Magnification 4000x; and (D) Fragment of adipocyte with peripherally located mitochondria showing signs of self-destruction (6), cell nucleus (8) with heterochromatin, and mast cell (9). a large fat droplet in an adipocyte (4) is also seen.…”

Section: Fig 4 Transmission Electron Microscopy Of Connective Tissumentioning

confidence: 99%

“…(С) Fragment of adipocyte with signs of fat defragmentation, large fat droplet (6), releasing fat droplets outside (8), damaged hemocapillary with signs of endothelial destruction (2), and edema between endothelium and basal membrane (7), 4000x magnification. (D) Fragment of adipocyte with the sign of digital-shaped invagination of the plasmalemma (9), cytoplasm (10) with a large number of self-destructive and ring-like mitochondria (4) located peripherally and large fat drop (6) defragmentation, releasing fat droplets outside (11), 4000x magnification the combination of ASA and NaHS -by 20% compared to vehicle (saline) treated rats (P < 0.001). Interestingly the level of TBARS during ASA pretreatment was increased by 15% compared to the vehicle (saline) group which had TBARS=6.41 µM/l (P < 0.001).…”

Section: Fig 3 Transmission Electron Microscopy Of the Mesentery Ofmentioning

confidence: 99%

“…Mesentery, one of the separate visceral organs that recently was discovered [6,7], serves functions in cross-talk of local or systemic responses via signaling pathways that play a crucial role in the induction of inflammatory factors, as well as control of glycemic and lipid metabolism [8,9]. Among different structural elements of the mesentery, there is white adipocyte tissue.…”

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confidence: 99%

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Novel approach for discrimination of eosinophilic granulocytes and evaluation of their surface receptors in a multicolor fluorescent histological assessment

Bila¹,

Schneider²,

Peshkova³

et al. 2020

Ukr.Biochem.J

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Remodeling of adipocytes in mesentery (aM) associated with nutritional overload from high fructose diet (hFD) is a source of several comorbidities. however, its pathogenesis is still unclear and there are no specific effective drugs for AM remodeling. Recently hydrogen sulfide (H 2 S) demonstrated potent cytoprotective actions. The purpose of this study was to investigate the effects and underlying mechanisms of AM remodeling in rats fed hFD and with h 2 S pre-treatment. adult male rats on standard diet (SD, control group) or hFD that underwent acute water-immersion restraint stress (WIS) were evaluated for subcellular aM adaptive responses by electron microscopy. The effects on AM of exogenous sodium hydrosulfide (NaHS, 5.6 mg/ kg/day for 9 days) and the Н 2 S-releasing aspirin (aSa) derivative (h 2 S-ASA , 17.5 mg/kg/day) vs conventional ASA (10 mg/kg/day) vs vehicle were investigated. Serum glucose level, thiobarbituric acid reactive substances (TBARS), and activities of cystathionine γ-lyase (CSE) and cystathionine β-synthase (CBS) were examined biochemically using spectrophotometry. In the HFD groups, treatment with NaHS protected aM, as mesenteric microvascular endothelial and sub-endothelial structures were observed vs the vehicletreated group that had signs of endothelial dysfunction, aM damage and dysfunctional mitochondria. The effect of H 2 S-aSa was characterized by protection of aM against hFD and WIS-induced injury, with lower TBARS blood level and increased CSE and CBS activities. Carbohydrate overload for 4 weeks is sufficient to cause AM oxidative damage, mitochondrial dysfunction and endothelial changes. H 2 S plays an important role in mesenteric adipocyte cellular survival against HFD-induced oxidative stress by decreasing overproduction of TBaRS and mitochondrial dysfunction. The use of h 2 S could lead to a novel approach for anti-obesity treatment.K e y w o r d s: hydrogen sulfide (H 2 S), thiobarbituric acid reactive substances (TBaRS), cystathionine gamma-lyase (CSE), cystathionine beta-synthase (CBS), oxidative stress, adipocytes, mesentery, mitochondria.

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“…Coffey and Rivera [ 90 , 91 ] gave other further hints to remove the veil of Maya on the pathogenesis and the mesenteric role. They started from the assumption that topographic distribution of Crohn’s disease along the intestinal tract may have a bodily mesenteric basis in terms of tissue volume and thickness.…”

Section: Por: New Discoveries and Trendsmentioning

confidence: 99%

Pathophysiology of Crohn’s disease inflammation and recurrence

et al. 2020

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Chron’s Disease is a chronic inflammatory intestinal disease, first described at the beginning of the last century. The disease is characterized by the alternation of periods of flares and remissions influenced by a complex pathogenesis in which inflammation plays a key role. Crohn’s disease evolution is mediated by a complex alteration of the inflammatory response which is characterized by alterations of the innate immunity of the intestinal mucosa barrier together with a remodeling of the extracellular matrix through the expression of metalloproteins and increased adhesion molecules expression, such as MAcCAM-1. This reshaped microenvironment enhances leucocytes migration in the sites of inflammation, promoting a TH1 response, through the production of cytokines such as IL-12 and TNF-α. IL-12 itself and IL-23 have been targeted for the medical treatment of CD. Giving the limited success of medical therapies, the treatment of the disease is invariably surgical. This review will highlight the role of inflammation in CD and describe the surgical approaches for the prevention of the almost inevitable recurrence.

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The Mesentery, Systemic Inflammation, and Crohn’s Disease

Abstract: 10.1093/ibd/izy201_video1izy201.video15794169491001.

Cited by 74 publications

References 71 publications

Difference in the frequency of pouchitis between ulcerative colitis and familial adenomatous polyposis: is the explanation in peripouch fat?

Difference in the frequency of pouchitis between ulcerative colitis and familial adenomatous polyposis: is the explanation in peripouch fat?

Novel approach for discrimination of eosinophilic granulocytes and evaluation of their surface receptors in a multicolor fluorescent histological assessment

Pathophysiology of Crohn’s disease inflammation and recurrence

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