Stricture of ileo-anal J pouch anastomosis increased the intensity of pouchitis in an experimental rat model

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Summary

Background

Pouchitis appears to be the most common complication after restorative proctocolectomy.

Material/Methods

In experimental models we investigated the correlation between the width of anastomosis and the frequency of pouchitis. Twenty-three Wistar rats underwent restorative proctocolectomy under pentobarbital anesthesia. Normal width anastomosis was performed in 11 animals (Group I). In the remaining 12 animals (Group II) the diameter of anastomosis was reduced by 50%. All animals were sacrificed and the pouch mucosa was histologically (Moskowitz score) and immunohistochemically (IL-1, IL-6, IL-10, IL-12 expression) examined.

Results

Morphological assessment of pouchitis symptoms based on Moskowitz scale revealed considerably more severe inflammation (p=0.0079) in the animals from Group II than in the rats from Group I. The expressions of investigated cytokines, assessed qualitatively in histopathological examination, were higher in rats with narrow anastomosis in comparison with animals with normal anastomosis.

Conclusions

The stricture of anastomosis increases the intensity of pouchitis and stimulates the production of interleukins. It seems that anastomotic stricture plays an important role in the development of pouchitis.

Related collections

Most cited references 27

Record: found
Abstract: found
Article: not found

Acute colitis induced by dextran sulfate sodium progresses to chronicity in C57BL/6 but not in BALB/c mice: correlation between symptoms and inflammation.

Silvia Melgar, Agneta Karlsson, Erik Michaëlsson (2005)

Exposure to dextran sulfate sodium (DSS) induces acute colitis, which is normally resolved after DSS removal. To study chronicity, mice are typically subjected to three to five cycles of weekly DSS exposures, each followed by a 1- to 2-wk rest period. Here, we describe a novel and convenient way of inducing chronic, progressive colitis by a single exposure to DSS. C57BL/6 mice exposed to DSS for 5 days developed acute colitis that progressed to severe chronic inflammation. The plasma haptoglobin levels remained high during the chronic phase, showing that the inflammation was active. Surprisingly, the mice regained their original weight along with the progression of colitis, and the only apparent symptom was loose feces. Histopathological changes 4 wk after DSS removal were dense infiltrates of mononuclear cells, irregular epithelial structure, and persistent deposits of collagen. A progressive production of the cytokines IL-1beta, IL-12 p70, and IL-17 correlated with the extensive cellular infiltration, whereas high IFN-gamma production was mainly found late in the chronic phase. Similar to C57BL/6 mice, BALB/c mice exposed to 5 days of DSS developed acute colitis as previously described. The acute colitis was accompanied by elevated plasma levels of haptoglobin and increased colonic levels of IL-1alpha/beta, IL-6, IL-18, and granulocyte colony-stimulating factor. However, soon after DSS removal, BALB/c mice recovered and were symptom free within 2 wk and completely recovered 4 wk after DSS removal in terms of histopathology, haptoglobin levels, and local cytokine production. In summary, these data stress the effect of genetic background on the outcome of DSS provocation. We believe that the present protocol to induce chronic colitis in C57BL/6 mice offers a robust model for validating future therapies for treatment of inflammatory bowel disease.

0 comments Cited 153 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Imbalance between interleukin-1 agonists and antagonists: relationship to severity of inflammatory bowel disease.

B. Siegmund, O Ludwiczek, I Borggraefe … (2004)

Interleukin (IL)-1 is a key mediator in the pathogenesis of inflammatory bowel disease (IBD). Naturally occurring IL-1 modulators include IL-1 receptor antagonist (IL-1Ra), IL-1 soluble receptor Type I (IL-1sRI), IL-1sRII and IL-1 receptor accessory protein (AcP). Systemic and mucosal levels of IL-1 soluble receptors remain unknown in IBD. Plasma or colonic tissues were obtained from 185 consecutive unselected patients with Crohn's disease (CD) or ulcerative colitis (UC) and from 52 control subjects. Plasma and colonic explant culture supernatants were assessed for IL-1alpha, IL-1beta, IL-1Ra, IL-1sRI and IL-1sRII. Plasma IL-1Ra levels were higher in UC (+93%) than in healthy subjects. IL-1alpha and IL-1beta were not detected. IL-1sRII levels were marginally lower in CD (-10%) and UC (-9%), whereas IL-1sRI levels were elevated in CD (+28%) only. Plasma IL-1sRI levels correlated positively (P < 0.01) with Crohn's disease activity index (r = 0.53), C-reactive protein (r = 0.46) and alpha1-acid glycoprotein (r = 0.42). In colonic explant cultures, IL-1alpha and IL-1Ra levels were elevated in non-lesional (+233% and +185% respectively) and lesional CD (+353% and +1069%), lesional UC (+604% and +1138%), but not in non-lesional UC. IL-1beta was elevated in lesional UC (+152%) and CD (+128%). In contrast, IL-1sRII levels were elevated in non-lesional CD (+65%), but remained unchanged in lesional CD, non-lesional and lesional UC. IL-1sRI levels did not differ between patient and control groups. These results indicate that (i) the proinflammatory moiety IL-1sRI is a systemic marker of inflammation and activity in CD and (ii) local shedding of the functional antagonist IL-1sRII may dampen colonic inflammation in CD, but not in UC.

0 comments Cited 48 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Essential roles of high-mobility group box 1 in the development of murine colitis and colitis-associated cancer.

Tomoya Ohmae, Shin Maeda, Wataru Shibata … (2007)

High-mobility group box 1 (HMGB1) is a nuclear factor released extracellularly as a proinflammatory cytokine. We measured the HMGB1 concentration in the sera of mice with chemically induced colitis (DSS; dextran sulfate sodium salt) and found a marked increase. Inhibition of HMGB1 by neutralizing anti-HMGB1 antibody resulted in reduced inflammation in DSS-treated colons. In macrophages, HMGB1 induces several proinflammatory cytokines, such as IL-6, which are regulated by NF-kappaB activation. Two putative sources of HMGB1 were explored: in one, bacterial factors induce HMGB1 secretion from macrophages and in the other, necrotic epithelial cells directly release HMGB1. LPS induced a small amount of HMGB1 in macrophages, but macrophages incubated with supernatant prepared from necrotic cells and containing large amounts of HMGB1 activated NF-kappaB and induced IL-6. Using the colitis-associated cancer model, we demonstrated that neutralizing anti-HMGB1 antibody decreases tumor incidence and size. These observations suggest that HMGB1 is a potentially useful target for IBD treatment and the prevention of colitis-associated cancer.

0 comments Cited 37 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Journal

Journal ID (nlm-ta): Med Sci Monit

Journal ID (iso-abbrev): Med. Sci. Monit

Journal ID (publisher-id): Medical Science Monitor

Title: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

Publisher: International Scientific Literature, Inc.

ISSN (Print): 1234-1010

ISSN (Electronic): 1643-3750

Publication date Collection: 2012

Publication date (Electronic): 01 October 2012

Volume: 18

Issue: 10

Pages: BR409-BR413

Affiliations

[1 ]Department of General Surgery, Gastroenterological Oncological Surgery and Plastic Surgery, K. Marcinkowski University of Medical Sciences, Poznan, Poland

[2 ]I Chair of Pediatrics, Department of Gastroenterology and Metabolism, K. Marcinkowski University of Medical Sciences, Poznan, Poland

[3 ]Department of Clinical Pathomorphology K. Marcinkowski University of Medical Sciences, Poznan, Poland

[4 ]Unit of General, Vascular and Oncological Surgery, Regional Hospital Slupsk

[5 ]Department of Oncological Surgery Medical University Gdansk, Gdansk, Poland

[6 ]Institute of Biomedicine, Division of Physiology and Biocenter Oulu, University of Oulu, Oulu, Finland

Author notes

Tomasz Banasiewicz, Department of General, Gastroenterological and Endocrinological Surgery, Przybyszewskiego 49 St., 60-355 Poznan, Poland, e-mail: tbanasiewicz@ 123456op.pl

[A]

Study Design

[B]

Data Collection

[C]

Statistical Analysis

[D]

Data Interpretation

[E]

Manuscript Preparation

[F]

Literature Search

[G]

Funds Collection

Article

Publisher ID: 883481

DOI: 10.12659/MSM.883481

PMC ID: 3560548

PubMed ID: 23018348

SO-VID: bd82568e-46b7-4b4b-8db1-e3a1db75b8d0

License:

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License.

History

Date received : 11 February 2012

Date accepted : 10 April 2012

Comments

Comment on this article

scite_

Smart Citations

Citing PublicationsSupportingMentioningContrasting

View Citations

See how this article has been cited at scite.ai

scite shows how a scientific paper has been cited by providing the context of the citation, a classification describing whether it supports, mentions, or contrasts the cited claim, and a label indicating in which section the citation was made.