Original Article
Copyright ©2014 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jul 7, 2014; 20(25): 8130-8138
Published online Jul 7, 2014. doi: 10.3748/wjg.v20.i25.8130
Phasic study of intestinal homeostasis disruption in experimental intestinal obstruction
Xiang-Yang Yu, Chang-Lin Zou, Zhen-Li Zhou, Tao Shan, Dong-Hua Li, Nai-Qiang Cui
Xiang-Yang Yu, Zhen-Li Zhou, Tao Shan, Department of Gastrointestinal Surgery, Nankai Hospital, Tianjin 300100, China
Chang-Lin Zou, Graduate School of Tianjin Medical University, Tianjin 300100, China
Dong-Hua Li, Tianjin Institute of Acute Abdominal Diseases of Integrated Traditional Chinese and Western Medicine, Tianjin 300100, China
Nai-Qiang Cui, Department of Hepatopancreatobiliary Surgery, Nankai Hospital, Tianjin 300100, China
Author contributions: Yu XY and Zou CL contributed equally to this study and performed the majority of the experiments; Zhou ZL, Shan T and Li DH participated in the performance of experiments; Yu XY and Cui NQ designed the study and wrote the manuscript.
Supported by National Program on Key Basic Research Project, No. 2009CB522703
Correspondence to: Xiang-Yang Yu, MD, Department of Gastrointestinal Surgery, Nankai Hospital, Nankai District, No. 6 Changjiang Rd, Tianjin 300100, China. yxynankai@126.com
Telephone: +86-22-27435860 Fax: +86-22-27435860
Received: September 3, 2013
Revised: February 21, 2014
Accepted: April 1, 2014
Published online: July 7, 2014
Processing time: 302 Days and 18.1 Hours
Abstract

AIM: To investigate the phasic alteration of intestinal homeostasis in an experimental model of intestinal obstruction.

METHODS: A rabbit model of intestinal obstruction was established by transforming parts of an infusion set into an in vivo pulled-type locking clamp and creating a uniform controllable loop obstruction in the mesenteric non-avascular zone 8 cm from the distal end of the ileum. The phasic alteration of intestinal homeostasis was studied after intestinal obstruction. The changes in goblet cells, intraepithelial lymphocytes, lamina propria lymphocytes, and intestinal epithelium were quantified from periodic acid-Schiff-stained sections. Ornithine decarboxylase (ODC) activity and serum citrulline levels were measured by high-performance liquid chromatography. Claudin 1 mRNA expression was examined by real-time polymerase chain reaction analysis. Intestinal microorganisms, wet/dry weight ratios, pH values, and endotoxin levels were determined at multiple points after intestinal obstruction. Furthermore, the number and ratio of CD3+, CD4+ and CD8+ T cells were determined by flow cytometry, and secretory IgA levels were measured with an enzyme-linked immunosorbent assay.

RESULTS: A suitable controllable rabbit model of intestinal obstruction was established. Intestinal obstruction induced goblet cell damage and reduced cell number. Further indicators of epithelial cell damage were observed as reduced serum citrulline levels and claudin 1 gene expression, and a transient increase in ODC activity. In addition, the wet/dry weight ratio and pH of the intestinal lumen were also dramatically altered. The ratio of Bacillus bifidus and enterobacteria was reversed following intestinal obstruction. The number and area of Peyer’s patches first increased then sharply decreased after the intestinal obstruction, along with an alteration in the ratio of CD4/CD8+ T cells, driven by an increase in CD3+ and CD8+ T cells and a decrease in CD4+ T cells. The number of lamina propria lymphocytes also gradually decreased with prolonged obstruction.

CONCLUSION: Intestinal obstruction can induce disruption of intestinal homeostasis.

Keywords: Intestinal obstruction; Rabbit model; Homeostasis disruption; Intestinal epithelial cells; Intestinal microorganisms; Intestinal immune system

Core tip: A controllable rabbit model of intestinal obstruction was established. This model demonstrated that intestinal obstruction (1) induced intestinal epithelial cell damage and reduction; (2) disrupted the balance of intestinal microorganisms by abnormal proliferation of pathogenic bacteria; and (3) disrupted the intestinal immune system, observed as a decrease in the number and area of Peyer’s patches, and alteration of CD4+ T cell number and CD4/CD8+ T cell ratio. Furthermore, the levels of ornithine decarboxylase activity and citrulline and claudin 1 expression could serve as indicators of intestinal epithelial cell damage.