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PubMed2005

Tissue models of peritoneal fibrosis.

OBJECTIVE: To evaluate the utility of peritoneal pathologic samples, unrelated to peritoneal dialysis (PD) treatment, for the study of peritoneal fibrosis and inflammation. METHODS: Comparative morphologic and immunohistochemical study of peritoneal pathologic samples unrelated to PD with peritoneal biopsies from PD patients with special emphasis on the expression of myofibroblastic and epithelial-to-mesenchymal transition markers. RESULTS: Regarding morphology, PD-related simple fibrosis was less cellular, with greater stromal hyalinization, determining a homogeneous, hypocellular aspect of the submesothelium. In contrast, non-PD fibrosis was more cellular with an extracellular matrix showing a dense and fibrillar quality with wide bundles of collagen. Hylinazing vasculopathy was only present in PD samples. Myofibroblastic differentiation and epithelial-to-mesenchymal transition were common findings in all situations of peritoneal fibrosis. Calponin and calretinin are useful cellular markers to study such fibrogenic mechanisms and correlate with other well-known markers such as a -SMA and cytokeratins. Their expression was much more intense in those samples showing acute inflammation (peritonitis). CONCLUSIONS: Non-PD models of peritoneal fibrosis seem very useful to evaluate important features of human peritoneal pathology such us fibrogenesis, and inflammation. Fibrogenic events such as myofibroblastic differentiation and epithelial-to-mesenchymal transition are evident in these tissue samples allowing us to use them as an accessible source for in vivo and ex vivo studies. Both events show their maximal expression in situations of acute inflammation supporting the important role that peritonitis episodes play in the progression of fibrosis.

Actins↗
PubMed2005

Possible effects of hepatocyte growth factor for the prevention of peritoneal fibrosis.

OBJECTIVE: Some patients who had carried out long-term continuous ambulatory peritoneal dialysis discontinued the treatment because of progressive peritoneal fibrosis. It has been previously reported that transforming growth factor-beta1 (TGF-beta1) is one of the factors that induces peritoneal fibrosis. Also, hepatocyte growth factor (HGF) plays a role in the prevention of fibrosis and in inhibiting TGF-beta1 production. In this study, we examined the effects of HGF on peritoneal fibrosis by TGF-beta1 induced by high concentrations of D-glucose. DESIGN: We transfected a full-length human HGF cDNA in an expression vector into human peritoneal mesothelial cells (HPMCs) using the calcium phosphate method. Transfected HPMCs were cultured with high concentrations of D-glucose solution and co-cultured with fibroblasts using a transwell system. Cell proliferation was determined using the Tetra Color One method. TGF-beta1 and HGF protein were measured by enzyme-linked immunosorbent assay. RESULTS: In addition to recombinant HGF, the growth inhibition of HPMCs by high concentration D-glucose or TGF-beta1 was significant. By transfecting HGF cDNA into HPMCs, growth inhibition by high concentration D-glucose was completely restored. Furthermore, the production of TGF-beta1 was also significantly decreased. CONCLUSION: These results suggested that exogenous HGF could possibly prevent peritoneal fibrosis.

Cell Proliferation↗
PubMed2005

[Comparision of several different peritoneal fibrosis rat models].

OBJECTIVE: To compare different types of peritoneal fibrosis models in rats. METHODS: Thirty-four SD rats were divided into 5 groups: control group (Group 1), normal saline group (Group 2), high glucose group (4.25% peritoneal dialysate, 4.25% PDF, Group 3), high glucose + lipopolysaceharides (LPS) group (4.25% PDF + LPS, Group 4), high glucose + erythromycin group (4.25% PDF + lactobionate erythromycin, Group 5). A 2-hour peritoneal equilibration test (PET) was performed after 5 weeks. Then animals were humanely killed. Dialysate-to-plasma urea ratio (D/ Purea), glucose reabsorption (D2/D0), net ultrafiltration (UF) volume were determined. The level of fibronectin in peritoneal tissues was measured by immunohistochemical method. Peritoneal membrane histology was evaluated by light microscopy. RESULTS: The D2/D0 ratio and net ultrafiltration volume in Groups 3, 4, and 5 were significantly lower than those in Groups 1 and 2 (P < 0.05) . The D/Purea ratio in Groups 3, 4 and 5 were significantly higher than that in Groups 1 and 2 (P < 0. 05 ). The level of fibronectin in Groups 3, 4 and 5 were significantly higher than that in Groups 1 and 2 (P < 0.05 ). CONCLUSION: Different types of peritoneal fibrosis models in rats has been established. The best model is high clusion glucose + erythromycin.

Animals↗
PubMed2004

The gene transfer of soluble VEGF type I receptor (Flt-1) attenuates peritoneal fibrosis formation in mice but not soluble TGF-beta type II receptor gene transfer.

Peritoneal fibrosis formation is a consequence of inflammation/injury and a significant medical problem to be solved. The effects of soluble VEGF receptor type I (sFlt-1) gene transfer on experimental peritoneal fibrosis were examined and compared with soluble transforming growth factor-beta (TGF-beta) receptor type II (sTGF beta RII) gene transfer. Male C57BL/6 mice were injected with 1.5 x 10(8) plaque-forming unit of adenovirus encoding active TGF-beta (AdTGF beta) intraperitoneally. Some mice had been treated with sTGF betaRII or sFlt-1 plasmid injection into skeletal muscle with electroporation 4 days before virus administration. Mice were euthanized at day 14 after virus administration. AdTGF beta induced significant elevation of serum active TGF-beta, caused significant inflammatory response [weight loss, elevation of serum amyloid-P (SAP) and IL-12, increased expression of monocyte chemoattractant protein-1 (MCP-1) mRNA], and induced marked thickening of the peritoneum and collagen deposition. Gene transfer of sFlt-1 reduced the collagen deposition approximately 81% in mesenteric tissue. Treatment with sFlt-1 decreased ICAM-1 and MCP-1 mRNA expression significantly. Significant negative correlation between serum sFlt-1 and placental growth factor level was observed, whereas there was no significant negative correlation between sFlt-1 and VEGF. On the other hand, sTGF beta RII treatment enhanced the AdTGF beta-induced inflammation (significant elevation of SAP, TNF-alpha, and IL-12 levels and upregulation of ICAM-1 and MCP-1 mRNA expressions) and failed to prevent collagen deposition. These observations indicate that sFlt-1 gene transfer might be of therapeutic benefit in peritoneal fibrosis.

Animals↗
PubMed1996

Peritoneal fibrosis in cirrhotics treated with peritoneovenous shunting for ascites. An autopsy study with clinical correlations.

Of 554 cirrhotics autopsied during 1975-1993, 69 had had peritoneovenous shunts. Generalized peritoneal fibrosis with cocoon formation was found in 26 (38%) of those with shunts but in only one of 485 without shunts (P = 0.00002). In 14/26 the fibrosis was asymptomatic, an incidental autopsy finding. Intestinal obstruction in 12/26 (46%), the only symptomatic manifestation, was fatal in five. The etiology of peritoneal fibrosis in shunted patients is unknown. The 26 patients with fibrosis had more prior abdominal operations, complicated abdominal wall hernias, and active biliary tract inflammations; the features differentiated them from the 43 patients without fibrosis. Scores in a 'peritoneal complication index,' that considered multiple risks in the same patients, were significantly higher in those with fibrosis. In addition to these peritoneal injuries or inflammations, the faster ascitic fluid circulation in shunted patients may have increased deposition of fibrin upon the peritoneum. Fibrogenic cytokines, thus spread throughout the abdomen from local sites, may have converted fibrinous adhesions to generalized peritoneal fibrosis.

Ascites↗
PubMed1995

Rat model of peritoneal fibrosis: preliminary observations.

The aim of this study was to establish a rat model of peritoneal fibrosis. After insertion of peritoneal catheters into 18 rats, the rats were divided into three groups. All animals were dialyzed twice a day with 4.25% Dianeal containing heparin. Group 1 rats (control) received antibiotics (vancomycin and gentamicin) in each exchange: group 2 rats were inoculated with Escherichia coli (5 x 10(6) in 5 mL of saline) at the beginning of the study; group 3 rats were treated with antibiotics after Escherichia coli inoculation; they also received a second inoculation of Escherichia coli after the second week of the study. By the end of the second week, group 2 rats were sacrificed because of catheter problems. Group 1 and 3 rats were sacrificed after 4 weeks of dialysis. A weekly peritoneal equilibration test (PET) was performed in each rat. The comparison of the PET results from the beginning and end of the study showed an increased permeability to glucose (p < 0.05) and total protein (p < 0.05) in group 3, which was not noted in group 1. In histology samples there was only delicate fibrosis with cellular infiltration in the peritoneum in group 1 rats. These changes were much more prominent in group 3 rats. This study suggests that E. coli peritonitis causes peritoneal fibrosis in rats, but to have a sclerosing encapsulating peritonitis (SEP) model this experiment must be carried out for a longer time.

Animals↗
PubMed1981

Peritoneal fibrosis due to practolol. Scanning electron microscopical and histological observations.

Three cases of peritoneal fibrosis induced by the beta adrenoceptor blocking agent practolol are presented. Histological and scanning electron microscopical specimens showed a thick layer of loose connective tissue with collagen bundles and fibroblasts. No evidence of mesothelial cells with characteristic microvilli was found. The conclusion is drawn that the basic feature of practolol peritonitis is the destruction of the mesothelial membrane and a slowly progressive formation of loose connective tissue. The reason for the increased formation of connective tissue and the cause of the excessive activity of fibroblasts are discussed.

Aged↗
PubMed1993

Abdominal wall thickness as a means of assessing peritoneal fibrosis in mice.

Herein we describe a method for the quantitative assessment of connective tissue deposition within the peritoneal cavity. Female C57BL/6 mice (8-10 weeks) were given a single intraperitoneal injection of varying concentrations of talc (100 mg, 50 mg, 30 mg, 20 mg) in 1 ml of PBS or PBS alone. After 14 days, animals were killed. Adhesion formation was measured by the standard method of Myllârniemi et al. (1966), namely a gross visual inspection of the peritoneal cavity. This analysis gave a crude assessment of connective tissue deposition in the abdominal cavity but did not allow one to distinguish more subtle differences between intermediate dosage groups. In addition, a histological evaluation was performed. For the latter method, portions of the abdominal wall of mice were fixed and processed for histological analysis using Masson's Trichrome stain which allows for differentiation of connective tissue components. The thickness of connective tissue between the parietal peritoneum and the underlying abdominal wall muscle was measured. A dose-dependent increase in connective tissue deposition was observed in talc-treated animals compared to saline control animals. A differential cell count of the peritoneal exudate cells (PEC) showed that there was no change in cell populations in talc treated animals (compared to control animals). Given the above results, the measurement of connective tissue thickness was found to give the most accurate assessment of peritoneal fibrosis than other previously used methods.

Abdominal Muscles↗
PubMed1987

Development of peritoneal fibrosis occurs under the mesothelial cell layer.

This study was carried out in order to find out which part of the peritoneal wall reacts toward silica and produces peritoneal fibrosis. Colloidal silica was injected into the peritoneal cavity of rats to induce chemical peritonitis and frozen sections of the peritoneal wall were stained with specific antibodies toward type I and III collagens and fibronectin. A massive proliferation of granulation tissue was observed between the submesothelial and muscular layers within 48 hr visualized by prominent fibronectin staining. Type III collagen formed lamellar-like structures in the newly formed granulation tissue. The connective tissue reaction was extended into the underlying muscular tissue. Three weeks after silica injection the reactive granulation tissue exceeded the original peritoneum three- to fourfold in thickness. At this stage it contained extended fibrillar structures oriented perpendicular to the surface or muscular layers of the peritoneum. Type I collagen antibody was bound to the superficial cell layer in the control samples and in the early peritonitis whereas the entire granulation tissue was evenly stained at 3 weeks. Type III collagen antibody was bound to the surface layer of the peritoneum, granulation tissue, and perimysial connective tissue throughout the healing period. The results indicate that the peritoneal fibrotic process occurs under the thin peritoneal lining cell layer and on the surface of the muscle layer.

Animals↗
PubMed1992

Intestinal obstruction due to diffuse peritoneal fibrosis at 2 years after the successful treatment of malignant peritoneal mesothelioma with intraperitoneal mitoxantrone.

A 44-year-old man who had achieved a complete remission of malignant peritoneal mesothelioma after the intraperitoneal administration of 25 mg/m2 mitoxantrone presented with clinical and radiological signs of intestinal obstruction suggestive of recurrent disease at about 2 years following the initial treatment. However, laparotomy revealed extensive adhesive fibrosis but no sign of malignant mesothelioma. The peritoneal complications of intraperitoneal cytostatic treatment are discussed.

Adult↗
PubMed1991

Type I and III procollagens in CAPD: markers of peritoneal fibrosis.

The carboxyterminal propeptide of type I procollagen (PICP) and the aminoterminal propeptide of type III procollagen (PIIINP) are split products related to formation of granulation tissue. Local concentrations reflect the state of fibrosis activity. PICP and PIINP were measured in serum and dialysate from 13 CAPD patients. One patient had 5-fold higher PICP and 8-fold higher PIIINP in the dialysate than the 12 other patients receiving CAPD. One month after the samples were collected, the patient was taken off CAPD due to sclerosins peritonitis. Our observation indicates that determinations of PICP and PIIINP in the dialysate could be useful markers of peritoneal fibrosis.

Biomarkers↗