Fat-wrapping in Crohn's disease: Pathological basis and relevance to surgical practice

Sheehan, A. L.; Warren, Bryan F.; Gear, M. W. L.; Shepherd, N A

doi:10.1002/bjs.1800790934

Cited by 234 publications

(172 citation statements)

References 11 publications

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“…These Crohn's disease lesions involve the intestinal serosa and mesentery. The characteristic changes in the serosal surface, including fat wrapping, correlate directly with overall extent of inflammatory changes: the stricture of the intestine (10,11), the depth of lymphoid aggregate penetration, and the number of lymphoid aggregates in the underlying ileal wall (12). These observations suggest that inflammation of viscera is not limited to the organ, but provokes responses in the peritoneal cavity as well.…”

Section: Inhibition Of Ccl1-ccr8 Interaction Prevents Aggregation Of mentioning

confidence: 93%

Inhibition of CCL1-CCR8 Interaction Prevents Aggregation of Macrophages and Development of Peritoneal Adhesions

Hoshino¹,

Kawamura²,

Yasuhara

et al. 2007

The Journal of Immunology

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Peritoneal adhesions are a significant complication of surgery and visceral inflammation; however, the mechanism has not been fully elucidated. The aim of this study was to clarify the mechanism of peritoneal adhesions by focusing on the cell trafficking and immune system in the peritoneal cavity. We investigated the specific recruitment of peritoneal macrophages (PMφ) and their expression of chemokine receptors in murine models of postoperative and postinflammatory peritoneal adhesions. PMφ aggregated at the site of injured peritoneum in these murine models of peritoneal adhesions. The chemokine receptor CCR8 was up-regulated in the aggregating PMφ when compared with naive PMφ. The up-regulation of CCR8 was also observed in PMφ, but not in bone marrow-derived Mφ, treated with inflammatory stimulants including bacterial components and cytokines. Importantly, CCL1, the ligand for CCR8, a product of both PMφ and peritoneal mesothelial cells (PMCs) following inflammatory stimulation, was a potent enhancer of CCR8 expression. Cell aggregation involving PMφ and PMCs was induced in vitro in the presence of CCL1. CCL1 also up-regulated mRNA levels of plasminogen activator inhibitor-1 in both PMφ and PMCs. CCR8 gene-deficient mice or mice treated with anti-CCL1-neutralizing Ab exhibited significantly reduced postoperational peritoneal adhesion. Our study now establishes a unique autocrine activation system in PMφ and the mechanism for recruitment of PMφ together with PMCs via CCL1/CCR8, as immune responses of peritoneal cavity, which triggers peritoneal adhesions.

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Section: Inhibition Of Ccl1-ccr8 Interaction Prevents Aggregation Of mentioning

confidence: 93%

Inhibition of CCL1-CCR8 Interaction Prevents Aggregation of Macrophages and Development of Peritoneal Adhesions

Hoshino¹,

Kawamura²,

Yasuhara

et al. 2007

The Journal of Immunology

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“…• The findings of increased adipose tissue in intestinal segments in patients with Crohn's disease, known as "fat wrapping," have clearly shown that inflammation plays an important role [17,[26][27].…”

Section: Excess Subcutaneous Adiposity and Chronic Lymphedemamentioning

confidence: 99%

Liposuction Normalizes – in Contrast to Other Therapies – Lymphedema-Induced Adipose Tissue Hypertrophy

Brorson

2013

Handchir Mikrochir plast Chir

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The various types of treatment of lymphedema are under discussion and there has been some controversy regarding liposuction for lymphedema. Although it is clear that conservative therapies such as complex decongestive therapy (CDT) and controlled compression therapy (CCT) should be tried in the first instance, options for the treatment of late-stage lymphedema that is not responding to such treatment is not so clear. Improvements in technique, patient preparation, and patient follow-up have led to a greater and a wider acceptance of liposuction as a treatment for lymphedema. This paper outlines the benefits of using liposuction and presents the evidence to support its use.

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“…Although this anomalous hypertrophy of adipose tissue appears to be a primary defect in Crohn's disease (Sheehan et al 1992;Desreumaux et al 1999), it has not featured prominently in the extensive, and in many cases sophisticated, research into its pathology. Of more than 6000 papers about Crohn's disease published during the last 20 years, only eleven (less than 0·2 %) mention adipose tissue.…”

Section: Crohn's Diseasementioning

confidence: 99%

Long-term changes in adipose tissue in human disease

Pond

2001

Proc. Nutr. Soc.

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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.

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Fat-wrapping in Crohn's disease: Pathological basis and relevance to surgical practice

Cited by 234 publications

References 11 publications

Inhibition of CCL1-CCR8 Interaction Prevents Aggregation of Macrophages and Development of Peritoneal Adhesions

Inhibition of CCL1-CCR8 Interaction Prevents Aggregation of Macrophages and Development of Peritoneal Adhesions

Liposuction Normalizes – in Contrast to Other Therapies – Lymphedema-Induced Adipose Tissue Hypertrophy

Long-term changes in adipose tissue in human disease

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