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PubMed1989

[An experimental study on mesenteritis and deformities of the intestinal canal; with special reference to the changes with time of deformities (angulation, distortion, coil-like appearance)].

1. The relationship of the mesenteric inflammation with intestinal loop deformities was made clear and changes of these deformities were examined with time, using experimental model rabbits. 2. The above rabbit was laparotomized and was caused to develop mesenteritis by applying acetic acid onto sigmoid mesentery and descending colic mesentery, then the abdomen was closed. Subjects were divided into 2 groups (A and B); A group and B group were re-laparotomized 3-7 and 21 days later, respectively and were observed for mesentery and loop appearance, then were extirpated for sigmoid colon and descending colon with mesenterium attached thereto. Roentgenograms were taken first with attachment of mesentery, secondly there-without. Then, the intestinal canal was opened and the mucosal surface was observed, together with bleeding and blood flow disturbance in the depth of the wall in transmitted light. 3. As a result, the following conclusions were obtained: 1) Macroscopically, mesentery was marked with redness for A group and with thickening and twitch due to cicatricial contraction for B group. 2) A group near to the third day showed remarkable shortening, narrowing and marginal irregularity of the loop, which disappeared with time and were scarcely observed for B group; these deformities were considered to involve mesenteric inflammations and ischemia caused by secondary blood flow disturbance. 3) A group near to the 7th day and B group showed remarkable angulation, distortion and coil-like appearance; these deformities are considered to have been caused by thickening (stiffness) of the mesentery and its attachment and twitch-distortion due to cicatricial contraction. 4) Coil-like appearance disappeared upon cutting off the mesentery from the loop.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Human intestinal lamina propria and intraepithelial lymphocytes express receptors specific for chemokines induced by inflammation.

To determine which chemokine receptors might be involved in T lymphocyte localization to the intestinal mucosa, we examined receptor expression on human intestinal lamina propria lymphocytes (LPL), intraepithelial lymphocytes (IEL) and CD45RO+beta7hi gut homing peripheral blood lymphocytes (PBL). Virtually all LPL and IEL expressed CXCR3 and CCR5, receptors that have been associated with Th1(Tc1)/Th0 lymphocytes, while CCR3 and CCR4, receptors associated with Th2 (Tc2)lymphocytes, CCR7, CXCR1 and CXCR2 were not expressed. CXCR3 and CCR5 receptors were functional, as LPL and IEL migrated to their respective ligands I-TAC and RANTES. In addition, most alphaEbeta7- LPL and IEL expressed high levels of CCR2. While the majority of CD45RO(-)beta7hi PBL also expressed CXCR3 and CCR5, a proportion of these cells were CXCR3- and/or CCR5- and some expressed CCR4 and/or CCR7, indicating that lymphocytes recruited to the intestinal mucosa represent a subset of these cells. In summary, our results show that LPL and IEL within the normal intestine express a specific and similar array of chemokine receptors whose ligands are constitutively expressed in the intestinal mucosa and whose expression is up-regulated during intestinal inflammation. These results support the view that CXCR3, CCR5 and CCR2 may play an important role in lymphocyte localization within the intestinal mucosa.

Animals↗
PubMed2005

[New surgical strategy in gastroschisis: treatment simplification according to its physiopathology].

INTRODUCTION: Gastroschisis (GS) is a congenital abdominal wall defect that permits bowel exposure to amniotic fluid (AF). Intestinal damage is related to the chemical action of AF and constriction. After birth at term, a thickened intestinal wall with inflammation and, in some cases, intestinal atresias were observed. Surgical repair and intestinal reubication may be difficult, and thus staged silo repair could be necessary. These patients require a long hospital stay owing to bowel damage causing severe intestinal hypoperistalsis and poor absorptive capacity. Total parenteral nutrition (TPN) is required for a long period. OBJECTIVE: The aim of this prospective study is to evaluate the benefits of a preterm delivery to avoid bowel damage and its post-natal consequences. PATIENTS AND METHODS: Six cases of prenatally-diagnosed GS have been treated following a new strategy since July 2002. A preterm Cesarean section (c-section) delivery was programmed at 34-35 weeks of gestational age (GA). Some hours after birth, at bedside in the NICU, bowel reduction through the defect hole was performed under general anesthesia. This preterm group (PT) was compared the past 6 cases at term (AT) from January 1998 to July 2002. Macroscopic appearance, atresia existence, surgical technique, silo requirement, neonatal outcome, TPN and hospital stay were analyzed. RESULTS: All six cases AT (mean GA: 36.3 weeks) presented bowel inflammation and thickened wall. Only 2/6 cases allowed the intestine to be housed in a primary closure after laparotomy. 4/6 cases required staged silo repair. 1 patient presented intestinal atresia and other had perforations who died at 17 days of life from intestinal sepsis. Mean postoperative intubation period was 16.2 days. Mean TPN was 41.2 days and mean hospital stay 69.8 days. PT group was monitored by prenatal sonography seeking bowel sonolucency. After programmed PT c-section delivery (mean GA: 34.8 weeks) in all 6 cases, bowel loops presented normal appearance and intestinal thickening was absent, except in one case. No prematurity-related respiratory complications were observed. Easy bowel reduction without abdominal compression was performed in all cases. 1/6 cases required surgical release of occlusive intestinal adherence. Mean postoperative intubation period was 0.4 days (9.6 hours). Oral feeding was started at 6 days. Mean TPN was 13.4 days and mean hospital stay 28.6 days. CONCLUSIONS: The third trimester is a critical period for fetal bowel development. Intestinal damage rises with increasing exposure time to amniotic fluid. This strategy of preterm delivery for the treatment of GS avoids intestinal damage, prevents "peel" and intestinal atresia, renders surgical reduction easier, reduces the hypoperistalsis, need for TPN and hospital stay. Multidisciplinary coordination between obstetricians, neonatologists and pediatric surgeons is required.

Digestive System Surgical Procedures↗
PubMed1997

[Cellular immunity in patients with non-specific inflammatory bowel disease for an extended period after surgery].

The study was aimed at investigating the expression of HLA-DR, CD4, CD8, CD56 surface antigens on peripheral blood lymphocytes in patients with non-specific inflammatory bowel diseases in the period of 1-5 years after the surgical procedure. The percentage of rosette forming T-cells in the theophylline test and skin reaction to mycotic and bacterial antigens were assessed simultaneously. The experiment included group of 12 patients (aged 5-55), treated surgically because of Crohn's disease or ulcerative colitis. The lymphocytes' surface antigens were examined by means of monoclonal antibodies and the APAAP procedure. Significantly increased (p < 0.001) percentage of lymphocytes with HLA-DR surface antigens and significantly decreased (p < 0.002) percentage of lymphocytes with CD8 surface antigens were observed in patients with non-specific inflammatory bowel diseases. In 6 of 12 patients the skin test results were negative. The clinical symptoms, which may suggest the maintaining inflammation of the intestinal mucosa were found in 50% of patients examined after surgical procedure because of Crohn's disease. The results suggest there are significant disturbances of cellular immunoreactivity parameters in patients with non-specific inflammatory bowel diseases. It may be one of the causes, which maintain the chronic inflammation of the intestinal mucosa and favour disease recurrence. The cellular immunoreactivity disturbances demonstrated in this study may be the result of the still persisting intestinal mucosa. Inflammation, in spite of deficiency of synonymous clinical symptoms indicating the disease recurrence.

Adolescent↗
PubMed1998

Cell adhesion and migration. IV. Lymphocyte trafficking in the intestine and liver.

Naive lymphocytes patrol continuously between the blood and different lymphatic tissues to sample the whole body for foreign antigens. During inflammation, leukocyte recruitment into tissue is enhanced to promote the recruitment of a range of effector cells into the affected area. The complex recirculatory pathways that underlie this process are governed by adhesion receptors on blood-borne leukocytes and by their specific ligands expressed on the luminal aspect of endothelial cells lining the vessels. Gut-associated lymphatic tissues are positioned strategically at the major port of entry for foreign antigens. They form a functionally unified entity that utilizes both the afferent and efferent arms of the immune response to respond to the large array of antigens entering via the gut under normal conditions as well as during inflammation. Once antigens have been absorbed from the gut, they may enter the portal vein and the liver where the immune response can be further regulated by the resident immune cells of the liver. Thus the gut and liver form an important barrier to enteral antigens, and leukocyte recruitment to these sites will need to be carefully regulated to ensure effective immune surveillance. In this article, we describe the current concepts of lymphocyte adhesion in these two organs as revealed by animal models. Subsequently, we discuss how well these principles apply to the lymphocyte-endothelial cell interactions in humans and what additional insights can be obtained from human studies.

Cell Adhesion↗
PubMed2006

Mast cell stabilizer ketotifen [4-(1-methyl-4-piperidylidene)-4h-benzo[4,5]cyclohepta[1,2-b]thiophen-10(9H)-one fumarate] prevents mucosal mast cell hyperplasia and intestinal dysmotility in experimental Trichinella spiralis inflammation in the rat.

Trichinella spiralis infection in rats induces hypermotility and an abnormal response to cholecystokinin (CCK) similar to motor disturbances observed in irritable bowel syndrome. Mast cell hyperplasia is also characteristic of this experimental model. The aim of our study was to correlate mast cell activity with the development of dysmotility and to demonstrate whether the mast cell stabilizer ketotifen [4-(1-methyl-4-piperidylidene)-4H-benzo[4,5]cyclohepta[1,2-b]thiophen-10(9H)-one fumarate] could prevent the development of intestine hypermotility. Sprague-Dawley rats were infected with T. spiralis and, 5 days after infection, treated with the mast-cell stabilizer ketotifen (10 mg/kg/day). Twelve days after infection, intestinal spontaneous motor activity and response to CCK were evaluated by means of strain-gauge transducers. Immunohistochemistry for rat mast cell protease II (RMCPII), cyclooxygenase (COX)-2, and inducible nitric-oxide synthase (iNOS) was performed in intestinal specimens. In addition, RMCPII and myeloperoxidase were determined in serum. Infected control rats showed hypermotility, mast cell hyperplasia, increased RMCPII levels, increased myeloperoxidase, and overexpression of COX-2 and iNOS. In contrast, ketotifen-treated rats showed spontaneous intestinal motility and CCK response similar to the noninfected control rats. Mast cell hyperplasia and RMCPII were reduced in ketotifen-treated rats. Inflammatory parameters were less modified by ketotifen, but those animals that received the longest ketotifen treatment showed a slight amelioration in these parameters. These results indicate that mast cells are implicated in the development of hypermotility. The treatment with ketotifen prevented hypermotility and mast cell hyperplasia and diminished mucosal mast cell activity.

Animals↗